[ { "key": "NPBI3SUR", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/NPBI3SUR", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/NPBI3SUR", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } }, "creatorSummary": "Feng et al.", "parsedDate": "2001-08-07", "numChildren": 0 }, "data": { "key": "NPBI3SUR", "version": 1, "itemType": "journalArticle", "title": "Increased inducible nitric oxide synthase expression contributes to myocardial dysfunction and higher mortality after myocardial infarction in mice", "creators": [ { "creatorType": "author", "firstName": "Q", "lastName": "Feng" }, { "creatorType": "author", "firstName": "X", "lastName": "Lu" }, { "creatorType": "author", "firstName": "D L", "lastName": "Jones" }, { "creatorType": "author", "firstName": "J", "lastName": "Shen" }, { "creatorType": "author", "firstName": "J M", "lastName": "Arnold" } ], "abstractNote": "BACKGROUND\n\nInducible nitric oxide synthase (iNOS) is expressed in the myocardium after myocardial infarction (MI) and in heart failure. Its pathophysiological role in these conditions, however, is not clear. We hypothesized that increased NO production from iNOS expression causes myocardial dysfunction and results in higher mortality after MI.\n\n\nMETHODS AND RESULTS\n\nMI was induced by left coronary artery ligation in iNOS(-/-) mutant and wild-type mice. Mortality was followed up for 30 days. MI resulted in a significant increase in mortality in both iNOS(-/-) and wild-type mice compared with sham operation (P<0.01). Mortality was significantly decreased and LV myocardial contractility was increased, however, in iNOS(-/-) mice compared with the wild-type mice (P<0.05). Five days after MI, myocardial iNOS mRNA expression, plasma nitrate and nitrite concentrations, and myocardial and plasma nitrotyrosine levels were significantly increased in wild-type compared with iNOS(-/-) mutant mice (P<0.05). Both basal LV +dP/dt and its response to dobutamine were significantly increased in iNOS(-/-) compared with the wild-type mice (P<0.05).\n\n\nCONCLUSIONS\n\nIncreased NO production from iNOS expression contributes to myocardial dysfunction and mortality after MI in mice.", "publicationTitle": "Circulation", "publisher": "", "place": "", "date": "Aug 7, 2001", "volume": "104", "issue": "6", "section": "", "partNumber": "", "partTitle": "", "pages": "700-704", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circulation", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/11489778", "accessDate": "2012-05-01T18:00:05Z", "PMID": "", "PMCID": "", "ISSN": "1524-4539", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 11489778", "tags": [ { "tag": "Animals", "type": 1 }, { "tag": "Female", "type": 1 }, { "tag": "Gene Expression Regulation, Enzymologic", "type": 1 }, { "tag": "Genotype", "type": 1 }, { "tag": "Heart Ventricles", "type": 1 }, { "tag": "Hemodynamics", "type": 1 }, { "tag": "Male", "type": 1 }, { "tag": "Mice", "type": 1 }, { "tag": "Mice, Inbred C57BL", "type": 1 }, { "tag": "Mice, Mutant Strains", "type": 1 }, { "tag": "Myocardial Contraction", "type": 1 }, { "tag": "Myocardial Infarction", "type": 1 }, { "tag": "Nitrates", "type": 1 }, { "tag": "Nitric Oxide Synthase", "type": 1 }, { "tag": "Nitric Oxide Synthase Type II", "type": 1 }, { "tag": "Nitric oxide", "type": 1 }, { "tag": "Nitrites", "type": 1 }, { "tag": "RNA, Messenger", "type": 1 }, { "tag": "Survival Rate", "type": 1 }, { "tag": "Time Factors", "type": 1 }, { "tag": "Tyrosine", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T18:00:05Z", "dateModified": "2012-05-01T18:00:05Z" } }, { "key": "G75AXZQG", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/G75AXZQG", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/G75AXZQG", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900980, "username": "cjc2nd", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/cjc2nd", "type": "text/html" } } }, "creatorSummary": "Feng et al.", "parsedDate": "2001-08-07", "numChildren": 0 }, "data": { "key": "G75AXZQG", "version": 1, "itemType": "journalArticle", "title": "Increased inducible nitric oxide synthase expression contributes to myocardial dysfunction and higher mortality after myocardial infarction in mice", "creators": [ { "creatorType": "author", "firstName": "Q", "lastName": "Feng" }, { "creatorType": "author", "firstName": "X", "lastName": "Lu" }, { "creatorType": "author", "firstName": "D L", "lastName": "Jones" }, { "creatorType": "author", "firstName": "J", "lastName": "Shen" }, { "creatorType": "author", "firstName": "J M", "lastName": "Arnold" } ], "abstractNote": "BACKGROUND\n\nInducible nitric oxide synthase (iNOS) is expressed in the myocardium after myocardial infarction (MI) and in heart failure. Its pathophysiological role in these conditions, however, is not clear. We hypothesized that increased NO production from iNOS expression causes myocardial dysfunction and results in higher mortality after MI.\n\n\nMETHODS AND RESULTS\n\nMI was induced by left coronary artery ligation in iNOS(-/-) mutant and wild-type mice. Mortality was followed up for 30 days. MI resulted in a significant increase in mortality in both iNOS(-/-) and wild-type mice compared with sham operation (P<0.01). Mortality was significantly decreased and LV myocardial contractility was increased, however, in iNOS(-/-) mice compared with the wild-type mice (P<0.05). Five days after MI, myocardial iNOS mRNA expression, plasma nitrate and nitrite concentrations, and myocardial and plasma nitrotyrosine levels were significantly increased in wild-type compared with iNOS(-/-) mutant mice (P<0.05). Both basal LV +dP/dt and its response to dobutamine were significantly increased in iNOS(-/-) compared with the wild-type mice (P<0.05).\n\n\nCONCLUSIONS\n\nIncreased NO production from iNOS expression contributes to myocardial dysfunction and mortality after MI in mice.", "publicationTitle": "Circulation", "publisher": "", "place": "", "date": "Aug 7, 2001", "volume": "104", "issue": "6", "section": "", "partNumber": "", "partTitle": "", "pages": "700-704", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circulation", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/11489778", "accessDate": "2012-05-01T17:57:46Z", "PMID": "", "PMCID": "", "ISSN": "1524-4539", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 11489778", "tags": [ { "tag": "Genotype", "type": 1 }, { "tag": "Hemodynamics", "type": 1 }, { "tag": "Mice, Inbred C57BL", "type": 1 }, { "tag": "Mice, Mutant Strains", "type": 1 }, { "tag": "Nitrates", "type": 1 }, { "tag": "Nitric Oxide Synthase Type II", "type": 1 }, { "tag": "Nitrites", "type": 1 }, { "tag": "RNA, Messenger", "type": 1 }, { "tag": "Survival Rate", "type": 1 }, { "tag": "Time Factors", "type": 1 }, { "tag": "Tyrosine", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T17:57:46Z", "dateModified": "2012-05-01T17:57:46Z" } }, { "key": "AD6T3E8K", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/AD6T3E8K", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/AD6T3E8K", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } }, "creatorSummary": "Zhang et al.", "parsedDate": "2010-09-17", "numChildren": 0 }, "data": { "key": "AD6T3E8K", "version": 1, "itemType": "journalArticle", "title": "Increasing cardiac contractility after myocardial infarction exacerbates cardiac injury and pump dysfunction", "creators": [ { "creatorType": "author", "firstName": "Hongyu", "lastName": "Zhang" }, { "creatorType": "author", "firstName": "Xiongwen", "lastName": "Chen" }, { "creatorType": "author", "firstName": "Erhe", "lastName": "Gao" }, { "creatorType": "author", "firstName": "Scott M", "lastName": "MacDonnell" }, { "creatorType": "author", "firstName": "Wei", "lastName": "Wang" }, { "creatorType": "author", "firstName": "Mikhail", "lastName": "Kolpakov" }, { "creatorType": "author", "firstName": "Hiroyuki", "lastName": "Nakayama" }, { "creatorType": "author", "firstName": "Xiaoying", "lastName": "Zhang" }, { "creatorType": "author", "firstName": "Naser", "lastName": "Jaleel" }, { "creatorType": "author", "firstName": "David M", "lastName": "Harris" }, { "creatorType": "author", "firstName": "Yingxin", "lastName": "Li" }, { "creatorType": "author", "firstName": "Mingxin", "lastName": "Tang" }, { "creatorType": "author", "firstName": "Remus", "lastName": "Berretta" }, { "creatorType": "author", "firstName": "Annarosa", "lastName": "Leri" }, { "creatorType": "author", "firstName": "Jan", "lastName": "Kajstura" }, { "creatorType": "author", "firstName": "Abdelkarim", "lastName": "Sabri" }, { "creatorType": "author", "firstName": "Walter J", "lastName": "Koch" }, { "creatorType": "author", "firstName": "Jeffery D", "lastName": "Molkentin" }, { "creatorType": "author", "firstName": "Steven R", "lastName": "Houser" } ], "abstractNote": "RATIONALE\n\nMyocardial infarction (MI) leads to heart failure (HF) and premature death. The respective roles of myocyte death and depressed myocyte contractility in the induction of HF after MI have not been clearly defined and are the focus of this study.\n\n\nOBJECTIVES\n\nWe developed a mouse model in which we could prevent depressed myocyte contractility after MI and used it to test the idea that preventing depression of myocyte Ca(2+)-handling defects could avert post-MI cardiac pump dysfunction.\n\n\nMETHODS AND RESULTS\n\nMI was produced in mice with inducible, cardiac-specific expression of the β2a subunit of the L-type Ca(2+) channel. Myocyte and cardiac function were compared in control and β2a animals before and after MI. β2a myocytes had increased Ca(2+) current; sarcoplasmic reticulum Ca(2+) load, contraction and Ca(2+) transients (versus controls), and β2a hearts had increased performance before MI. After MI, cardiac function decreased. However, ventricular dilation, myocyte hypertrophy and death, and depressed cardiac pump function were greater in β2a versus control hearts after MI. β2a animals also had poorer survival after MI. Myocytes isolated from β2a hearts after MI did not develop depressed Ca(2+) handling, and Ca(2+) current, contractions, and Ca(2+) transients were still above control levels (before MI).\n\n\nCONCLUSIONS\n\nMaintaining myocyte contractility after MI, by increasing Ca(2+) influx, depresses rather than improves cardiac pump function after MI by reducing myocyte number.", "publicationTitle": "Circulation Research", "publisher": "", "place": "", "date": "Sep 17, 2010", "volume": "107", "issue": "6", "section": "", "partNumber": "", "partTitle": "", "pages": "800-809", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circ. Res.", "DOI": "10.1161/CIRCRESAHA.110.219220", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/20671241", "accessDate": "2012-05-01T17:56:26Z", "PMID": "", "PMCID": "", "ISSN": "1524-4571", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 20671241", "tags": [ { "tag": "Animals", "type": 1 }, { "tag": "Calcium Channels, L-Type", "type": 1 }, { "tag": "Calcium Signaling", "type": 1 }, { "tag": "Cells, Cultured", "type": 1 }, { "tag": "Mice", "type": 1 }, { "tag": "Mice, Transgenic", "type": 1 }, { "tag": "Myocardial Contraction", "type": 1 }, { "tag": "Myocardial Infarction", "type": 1 }, { "tag": "Myocytes, Cardiac", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T17:56:26Z", "dateModified": "2012-05-01T17:56:26Z" } }, { "key": "3XS76FJ5", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/3XS76FJ5", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/3XS76FJ5", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900980, "username": "cjc2nd", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/cjc2nd", "type": "text/html" } } }, "creatorSummary": "Zhang et al.", "parsedDate": "2010-09-17", "numChildren": 0 }, "data": { "key": "3XS76FJ5", "version": 1, "itemType": "journalArticle", "title": "Increasing cardiac contractility after myocardial infarction exacerbates cardiac injury and pump dysfunction", "creators": [ { "creatorType": "author", "firstName": "Hongyu", "lastName": "Zhang" }, { "creatorType": "author", "firstName": "Xiongwen", "lastName": "Chen" }, { "creatorType": "author", "firstName": "Erhe", "lastName": "Gao" }, { "creatorType": "author", "firstName": "Scott M", "lastName": "MacDonnell" }, { "creatorType": "author", "firstName": "Wei", "lastName": "Wang" }, { "creatorType": "author", "firstName": "Mikhail", "lastName": "Kolpakov" }, { "creatorType": "author", "firstName": "Hiroyuki", "lastName": "Nakayama" }, { "creatorType": "author", "firstName": "Xiaoying", "lastName": "Zhang" }, { "creatorType": "author", "firstName": "Naser", "lastName": "Jaleel" }, { "creatorType": "author", "firstName": "David M", "lastName": "Harris" }, { "creatorType": "author", "firstName": "Yingxin", "lastName": "Li" }, { "creatorType": "author", "firstName": "Mingxin", "lastName": "Tang" }, { "creatorType": "author", "firstName": "Remus", "lastName": "Berretta" }, { "creatorType": "author", "firstName": "Annarosa", "lastName": "Leri" }, { "creatorType": "author", "firstName": "Jan", "lastName": "Kajstura" }, { "creatorType": "author", "firstName": "Abdelkarim", "lastName": "Sabri" }, { "creatorType": "author", "firstName": "Walter J", "lastName": "Koch" }, { "creatorType": "author", "firstName": "Jeffery D", "lastName": "Molkentin" }, { "creatorType": "author", "firstName": "Steven R", "lastName": "Houser" } ], "abstractNote": "RATIONALE\n\nMyocardial infarction (MI) leads to heart failure (HF) and premature death. The respective roles of myocyte death and depressed myocyte contractility in the induction of HF after MI have not been clearly defined and are the focus of this study.\n\n\nOBJECTIVES\n\nWe developed a mouse model in which we could prevent depressed myocyte contractility after MI and used it to test the idea that preventing depression of myocyte Ca(2+)-handling defects could avert post-MI cardiac pump dysfunction.\n\n\nMETHODS AND RESULTS\n\nMI was produced in mice with inducible, cardiac-specific expression of the β2a subunit of the L-type Ca(2+) channel. Myocyte and cardiac function were compared in control and β2a animals before and after MI. β2a myocytes had increased Ca(2+) current; sarcoplasmic reticulum Ca(2+) load, contraction and Ca(2+) transients (versus controls), and β2a hearts had increased performance before MI. After MI, cardiac function decreased. However, ventricular dilation, myocyte hypertrophy and death, and depressed cardiac pump function were greater in β2a versus control hearts after MI. β2a animals also had poorer survival after MI. Myocytes isolated from β2a hearts after MI did not develop depressed Ca(2+) handling, and Ca(2+) current, contractions, and Ca(2+) transients were still above control levels (before MI).\n\n\nCONCLUSIONS\n\nMaintaining myocyte contractility after MI, by increasing Ca(2+) influx, depresses rather than improves cardiac pump function after MI by reducing myocyte number.", "publicationTitle": "Circulation Research", "publisher": "", "place": "", "date": "Sep 17, 2010", "volume": "107", "issue": "6", "section": "", "partNumber": "", "partTitle": "", "pages": "800-809", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circ. Res.", "DOI": "10.1161/CIRCRESAHA.110.219220", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/20671241", "accessDate": "2012-05-01T17:55:51Z", "PMID": "", "PMCID": "", "ISSN": "1524-4571", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 20671241", "tags": [ { "tag": "Calcium Channels, L-Type", "type": 1 }, { "tag": "Calcium Signaling", "type": 1 }, { "tag": "Mice, Transgenic", "type": 1 }, { "tag": "Myocytes, Cardiac", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T17:55:51Z", "dateModified": "2012-05-01T17:55:51Z" } }, { "key": "PPAS3JCQ", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/PPAS3JCQ", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/PPAS3JCQ", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/EN2TB7I7", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } } }, "data": { "key": "PPAS3JCQ", "version": 1, "parentItem": "EN2TB7I7", "itemType": "attachment", "linkMode": "linked_url", "title": "ScienceDirect Snapshot", "accessDate": "2012-05-01T17:43:28Z", "url": "http://www.sciencedirect.com/science/article/pii/S0143416004000442", "note": "", "contentType": "text/html", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T17:43:28Z", "dateModified": "2012-05-01T17:43:28Z" } }, { "key": "5XS8FUHZ", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/5XS8FUHZ", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/5XS8FUHZ", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/EN2TB7I7", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } } }, "data": { "key": "5XS8FUHZ", "version": 1, "parentItem": "EN2TB7I7", "itemType": "attachment", "linkMode": "linked_url", "title": "ScienceDirect Full Text PDF", "accessDate": "2012-05-01T17:43:28Z", "url": "http://pdn.sciencedirect.com/science?_ob=MiamiImageURL&_cid=272490&_user=709071&_pii=S0143416004000442&_check=y&_origin=article&_zone=toolbar&_coverDate=31-Aug-2004&view=c&originContentFamily=serial&wchp=dGLzVlS-zSkzS&md5=8e56de9d6e13ffadf7fc4fa18969f9e5/1-s2.0-S0143416004000442-main.pdf", "note": "", "contentType": "application/pdf", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T17:43:28Z", "dateModified": "2012-05-01T17:43:28Z" } }, { "key": "EN2TB7I7", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/EN2TB7I7", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/EN2TB7I7", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } }, "creatorSummary": "Soloviev et al.", "parsedDate": "2004-08", "numChildren": 2 }, "data": { "key": "EN2TB7I7", "version": 1, "itemType": "journalArticle", "title": "Nitric oxide relaxes rat tail artery smooth muscle by cyclic GMP-independent decrease in calcium sensitivity of myofilaments", "creators": [ { "creatorType": "author", "firstName": "A.", "lastName": "Soloviev" }, { "creatorType": "author", "firstName": "V.", "lastName": "Lehen’kyi" }, { "creatorType": "author", "firstName": "S.", "lastName": "Zelensky" }, { "creatorType": "author", "firstName": "P.", "lastName": "Hellstrand" } ], "abstractNote": "The effects of authentic nitric oxide (NO, 10−6 M) and NO-donors such as sodium nitroprusside (SNP, 10−5 M) and glyceryl trinitrate (GTN, 10−4 M) on contractile force and free intracellular calcium level ([Ca2+]i) were studied on precontracted with high potassium chloride (KCl, 70 mM) isolated rings of rat tail artery. The sensitivity of contractile myofilaments to Ca2+ was measured using chemically permeabilized (α-toxin, β-escin, Triton X-100) vascular rings. [Ca2+]i and contractile activity were measured simultaneously. The relationship of [Ca2+]i and tension developed was studied in endothelium-denuded rings and controlled calcium response was evaluated in both endothelium-denuded and permeabilized vascular rings. Both authentic NO and NO-donors decreased [Ca2+]i and high potassium-induced tension with a different time course. Inhibitor of soluble guanylyl cyclase (sGC) LY83583 (10−5 M) did not affect SNP-induced relaxation whereas the other sGC inhibitor ODQ (10−6 M) attenuated SNP-induced relaxation. Both inhibitors had no effect on NO- and SNP-induced reduction in [Ca2+]i. On the contrary, GTN induced neither relaxation nor decrease in [Ca2+]i on application of both LY83583 and ODQ. Tail artery rings permeabilized with α-toxin, β-escin, but not with Triton X-100 were relaxed by authentic NO and NO-donors, but to a less extent than non-permeabilized rings. Dithioerythritol (DTE, 5×10−3 M) that maintains sulfhydryl (SH) groups in reduced state preventing their nitrosylation attenuated NO-induced relaxation in both non-permeabilized and permeabilized tail artery rings. The cyclic heptapeptide mycrocystin-LR (MC-LR) (10−5 M), an inhibitor of type 1 and 2A phosphatases, induced sustained increase in tension of β-escin permeabilized rings in low Ca2+ (10−8 M) solution. The tension was not affected by authentic NO and SNP. We conclude that authentic NO and SNP relax rat tail artery smooth muscle (SM) in the presence of inhibitors of sGC via cyclic guanosine monophosphate (cGMP)-independent pathway, whereas relaxation induced by GTN is inhibited. The data demonstrate that cGMP-dependent pathway in vascular smooth muscle is ubiquitous, but not the only way of relaxation induced by NO. NO can modulate vascular tone directly by reducing sensitivity of contractile myofilaments to [Ca2+]i and may involve activation of protein phosphatase(s).", "publicationTitle": "Cell Calcium", "publisher": "", "place": "", "date": "August 2004", "volume": "36", "issue": "2", "section": "", "partNumber": "", "partTitle": "", "pages": "165-173", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "", "DOI": "10.1016/j.ceca.2004.02.002", "citationKey": "", "url": "http://www.sciencedirect.com/science/article/pii/S0143416004000442", "accessDate": "2012-05-01T17:43:28Z", "PMID": "", "PMCID": "", "ISSN": "0143-4160", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "ScienceDirect", "callNumber": "", "rights": "", "extra": "", "tags": [ { "tag": "Cyclic guanosine monophosphate", "type": 1 }, { "tag": "Intracellular free calcium level", "type": 1 }, { "tag": "Myofilament calcium sensitivity", "type": 1 }, { "tag": "NO-donors", "type": 1 }, { "tag": "Nitric oxide", "type": 1 }, { "tag": "Soluble guanylyl cyclase", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T17:43:28Z", "dateModified": "2012-05-01T17:43:28Z" } }, { "key": "6MSFIZEV", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/6MSFIZEV", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/6MSFIZEV", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/RST8PJPN", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900980, "username": "cjc2nd", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/cjc2nd", "type": "text/html" } } } }, "data": { "key": "6MSFIZEV", "version": 1, "parentItem": "RST8PJPN", "itemType": "attachment", "linkMode": "linked_url", "title": "ScienceDirect Full Text PDF", "accessDate": "2012-05-01T17:41:54Z", "url": "http://www.sciencedirect.com/science?_ob=ShoppingCartURL&_method=add&_eid=1-s2.0-S0143416004000442&originContentFamily=serial&_origin=article&_acct=C000228598&_version=1&_userid=10&_ts=1335894104&md5=942cc6499878c3b77ef157678543a0ed", "note": "", "contentType": "application/pdf", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T17:41:54Z", "dateModified": "2012-05-01T17:41:54Z" } }, { "key": "RST8PJPN", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/RST8PJPN", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/RST8PJPN", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900980, "username": "cjc2nd", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/cjc2nd", "type": "text/html" } } }, "creatorSummary": "Soloviev et al.", "parsedDate": "2004-08", "numChildren": 2 }, "data": { "key": "RST8PJPN", "version": 1, "itemType": "journalArticle", "title": "Nitric oxide relaxes rat tail artery smooth muscle by cyclic GMP-independent decrease in calcium sensitivity of myofilaments", "creators": [ { "creatorType": "author", "firstName": "A.", "lastName": "Soloviev" }, { "creatorType": "author", "firstName": "V.", "lastName": "Lehen’kyi" }, { "creatorType": "author", "firstName": "S.", "lastName": "Zelensky" }, { "creatorType": "author", "firstName": "P.", "lastName": "Hellstrand" } ], "abstractNote": "The effects of authentic nitric oxide (NO, 10−6 M) and NO-donors such as sodium nitroprusside (SNP, 10−5 M) and glyceryl trinitrate (GTN, 10−4 M) on contractile force and free intracellular calcium level ([Ca2+]i) were studied on precontracted with high potassium chloride (KCl, 70 mM) isolated rings of rat tail artery. The sensitivity of contractile myofilaments to Ca2+ was measured using chemically permeabilized (α-toxin, β-escin, Triton X-100) vascular rings. [Ca2+]i and contractile activity were measured simultaneously. The relationship of [Ca2+]i and tension developed was studied in endothelium-denuded rings and controlled calcium response was evaluated in both endothelium-denuded and permeabilized vascular rings. Both authentic NO and NO-donors decreased [Ca2+]i and high potassium-induced tension with a different time course. Inhibitor of soluble guanylyl cyclase (sGC) LY83583 (10−5 M) did not affect SNP-induced relaxation whereas the other sGC inhibitor ODQ (10−6 M) attenuated SNP-induced relaxation. Both inhibitors had no effect on NO- and SNP-induced reduction in [Ca2+]i. On the contrary, GTN induced neither relaxation nor decrease in [Ca2+]i on application of both LY83583 and ODQ. Tail artery rings permeabilized with α-toxin, β-escin, but not with Triton X-100 were relaxed by authentic NO and NO-donors, but to a less extent than non-permeabilized rings. Dithioerythritol (DTE, 5×10−3 M) that maintains sulfhydryl (SH) groups in reduced state preventing their nitrosylation attenuated NO-induced relaxation in both non-permeabilized and permeabilized tail artery rings. The cyclic heptapeptide mycrocystin-LR (MC-LR) (10−5 M), an inhibitor of type 1 and 2A phosphatases, induced sustained increase in tension of β-escin permeabilized rings in low Ca2+ (10−8 M) solution. The tension was not affected by authentic NO and SNP. We conclude that authentic NO and SNP relax rat tail artery smooth muscle (SM) in the presence of inhibitors of sGC via cyclic guanosine monophosphate (cGMP)-independent pathway, whereas relaxation induced by GTN is inhibited. The data demonstrate that cGMP-dependent pathway in vascular smooth muscle is ubiquitous, but not the only way of relaxation induced by NO. NO can modulate vascular tone directly by reducing sensitivity of contractile myofilaments to [Ca2+]i and may involve activation of protein phosphatase(s).", "publicationTitle": "Cell Calcium", "publisher": "", "place": "", "date": "August 2004", "volume": "36", "issue": "2", "section": "", "partNumber": "", "partTitle": "", "pages": "165-173", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "", "DOI": "10.1016/j.ceca.2004.02.002", "citationKey": "", "url": "http://www.sciencedirect.com/science/article/pii/S0143416004000442", "accessDate": "2012-05-01T17:41:54Z", "PMID": "", "PMCID": "", "ISSN": "0143-4160", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "ScienceDirect", "callNumber": "", "rights": "", "extra": "", "tags": [ { "tag": "Cyclic guanosine monophosphate", "type": 1 }, { "tag": "Intracellular free calcium level", "type": 1 }, { "tag": "Myofilament calcium sensitivity", "type": 1 }, { "tag": "NO-donors", "type": 1 }, { "tag": "Soluble guanylyl cyclase", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T17:41:54Z", "dateModified": "2012-05-01T17:41:54Z" } }, { "key": "RAJC6TXI", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/RAJC6TXI", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/RAJC6TXI", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/RST8PJPN", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900980, "username": "cjc2nd", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/cjc2nd", "type": "text/html" } } } }, "data": { "key": "RAJC6TXI", "version": 1, "parentItem": "RST8PJPN", "itemType": "attachment", "linkMode": "linked_url", "title": "ScienceDirect Snapshot", "accessDate": "2012-05-01T17:41:54Z", "url": "http://www.sciencedirect.com/science/article/pii/S0143416004000442", "note": "", "contentType": "text/html", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T17:41:54Z", "dateModified": "2012-05-01T17:41:54Z" } }, { "key": "P2CEP2QH", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/P2CEP2QH", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/P2CEP2QH", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } }, "creatorSummary": "González et al.", "parsedDate": "2008-05", "numChildren": 0 }, "data": { "key": "P2CEP2QH", "version": 1, "itemType": "journalArticle", "title": "Differential role of S-nitrosylation and the NO-cGMP-PKG pathway in cardiac contractility", "creators": [ { "creatorType": "author", "firstName": "Daniel R", "lastName": "González" }, { "creatorType": "author", "firstName": "Ignacio C", "lastName": "Fernández" }, { "creatorType": "author", "firstName": "Pablo P", "lastName": "Ordenes" }, { "creatorType": "author", "firstName": "Adriana V", "lastName": "Treuer" }, { "creatorType": "author", "firstName": "Gisela", "lastName": "Eller" }, { "creatorType": "author", "firstName": "Mauricio P", "lastName": "Boric" } ], "abstractNote": "The role of nitric oxide (NO) in cardiac contractility is complex and controversial. Several NO donors have been reported to cause positive or negative inotropism. NO can bind to guanylate cyclase, increasing cGMP production and activating PKG. NO may also directly S-nitrosylate cysteine residues of specific proteins. We used the isolated rat heart preparation to test the hypothesis that the differential inotropic effects depend on the degree of NO production and the signaling recruited. SNAP (S-nitroso-N-acetylpenicillamine), a NO donor, increased contractility at 0.1, 1 and 10 microM. This effect was independent of phospholamban phosphorylation, was not affected by PKA inhibition with H-89 (N-[2((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide), but it was abolished by the radical scavenger Tempol (4-hydroxy-[2,2,4,4]-tetramethyl-piperidine-1-oxyl). However, at 100 microM SNAP reduced contractility, effect reversed to positive inotropism by guanylyl cyclase blockade with ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one), and abolished by PKG inhibition with KT5823, but not affected by Tempol. SNAP increased tissue cGMP at 100 microM, but not at lower concentrations. Consistently, a cGMP analog also reduced cardiac contractility. Finally, SNAP at 1 microM increased the level of S-nitrosylation of various cardiac proteins, including the ryanodine receptor. This study demonstrates the biphasic role for NO in cardiac contractility in a given preparation; furthermore, the differential effect is clearly ascribed to the signaling pathways involved. We conclude that although NO is highly diffusible, its output determines the fate of the messenger: low NO concentrations activate redox processes (S-nitrosylation), increasing contractility; while the cGMP-PKG pathway is activated at high NO concentrations, reducing contractility.", "publicationTitle": "Nitric Oxide: Biology and Chemistry / Official Journal of the Nitric Oxide Society", "publisher": "", "place": "", "date": "May 2008", "volume": "18", "issue": "3", "section": "", "partNumber": "", "partTitle": "", "pages": "157-167", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Nitric Oxide", "DOI": "10.1016/j.niox.2007.09.086", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/18023373", "accessDate": "2012-05-01T17:33:25Z", "PMID": "", "PMCID": "", "ISSN": "1089-8611", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 18023373", "tags": [ { "tag": "Animals", "type": 1 }, { "tag": "Calcium-Binding Proteins", "type": 1 }, { "tag": "Carbazoles", "type": 1 }, { "tag": "Cyclic GMP", "type": 1 }, { "tag": "Cyclic GMP-Dependent Protein Kinases", "type": 1 }, { "tag": "Cyclic N-Oxides", "type": 1 }, { "tag": "Male", "type": 1 }, { "tag": "Myocardial Contraction", "type": 1 }, { "tag": "Nitric oxide", "type": 1 }, { "tag": "Organ Culture Techniques", "type": 1 }, { "tag": "Rats", "type": 1 }, { "tag": "Rats, Sprague-Dawley", "type": 1 }, { "tag": "S-Nitroso-N-Acetylpenicillamine", "type": 1 }, { "tag": "Signal Transduction", "type": 1 }, { "tag": "Spin Labels", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T17:33:25Z", "dateModified": "2012-05-01T17:33:25Z" } }, { "key": "37CR4NXN", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/37CR4NXN", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/37CR4NXN", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900980, "username": "cjc2nd", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/cjc2nd", "type": "text/html" } } }, "creatorSummary": "González et al.", "parsedDate": "2008-05", "numChildren": 0 }, "data": { "key": "37CR4NXN", "version": 1, "itemType": "journalArticle", "title": "Differential role of S-nitrosylation and the NO-cGMP-PKG pathway in cardiac contractility", "creators": [ { "creatorType": "author", "firstName": "Daniel R", "lastName": "González" }, { "creatorType": "author", "firstName": "Ignacio C", "lastName": "Fernández" }, { "creatorType": "author", "firstName": "Pablo P", "lastName": "Ordenes" }, { "creatorType": "author", "firstName": "Adriana V", "lastName": "Treuer" }, { "creatorType": "author", "firstName": "Gisela", "lastName": "Eller" }, { "creatorType": "author", "firstName": "Mauricio P", "lastName": "Boric" } ], "abstractNote": "The role of nitric oxide (NO) in cardiac contractility is complex and controversial. Several NO donors have been reported to cause positive or negative inotropism. NO can bind to guanylate cyclase, increasing cGMP production and activating PKG. NO may also directly S-nitrosylate cysteine residues of specific proteins. We used the isolated rat heart preparation to test the hypothesis that the differential inotropic effects depend on the degree of NO production and the signaling recruited. SNAP (S-nitroso-N-acetylpenicillamine), a NO donor, increased contractility at 0.1, 1 and 10 microM. This effect was independent of phospholamban phosphorylation, was not affected by PKA inhibition with H-89 (N-[2((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide), but it was abolished by the radical scavenger Tempol (4-hydroxy-[2,2,4,4]-tetramethyl-piperidine-1-oxyl). However, at 100 microM SNAP reduced contractility, effect reversed to positive inotropism by guanylyl cyclase blockade with ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one), and abolished by PKG inhibition with KT5823, but not affected by Tempol. SNAP increased tissue cGMP at 100 microM, but not at lower concentrations. Consistently, a cGMP analog also reduced cardiac contractility. Finally, SNAP at 1 microM increased the level of S-nitrosylation of various cardiac proteins, including the ryanodine receptor. This study demonstrates the biphasic role for NO in cardiac contractility in a given preparation; furthermore, the differential effect is clearly ascribed to the signaling pathways involved. We conclude that although NO is highly diffusible, its output determines the fate of the messenger: low NO concentrations activate redox processes (S-nitrosylation), increasing contractility; while the cGMP-PKG pathway is activated at high NO concentrations, reducing contractility.", "publicationTitle": "Nitric Oxide: Biology and Chemistry / Official Journal of the Nitric Oxide Society", "publisher": "", "place": "", "date": "May 2008", "volume": "18", "issue": "3", "section": "", "partNumber": "", "partTitle": "", "pages": "157-167", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Nitric Oxide", "DOI": "10.1016/j.niox.2007.09.086", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/18023373", "accessDate": "2012-05-01T17:30:21Z", "PMID": "", "PMCID": "", "ISSN": "1089-8611", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 18023373", "tags": [ { "tag": "Calcium-Binding Proteins", "type": 1 }, { "tag": "Carbazoles", "type": 1 }, { "tag": "Cyclic N-Oxides", "type": 1 }, { "tag": "Myocardial Contraction", "type": 1 }, { "tag": "Organ Culture Techniques", "type": 1 }, { "tag": "Spin Labels", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T17:30:21Z", "dateModified": "2012-05-01T17:30:21Z" } }, { "key": "7R5TTJVT", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/7R5TTJVT", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/7R5TTJVT", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/NZXJBCMJ", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900980, "username": "cjc2nd", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/cjc2nd", "type": "text/html" } } } }, "data": { "key": "7R5TTJVT", "version": 1, "parentItem": "NZXJBCMJ", "itemType": "attachment", "linkMode": "linked_url", "title": "PLoS Full Text PDF", "accessDate": "2012-05-01T17:26:51Z", "url": "http://www.plosone.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0011209&representation=PDF", "note": "", "contentType": "application/pdf", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T17:26:51Z", "dateModified": "2012-05-01T17:26:51Z" } }, { "key": "NZXJBCMJ", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/NZXJBCMJ", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/NZXJBCMJ", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900980, "username": "cjc2nd", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/cjc2nd", "type": "text/html" } } }, "creatorSummary": "Evangelista et al.", "parsedDate": "2010-06-18", "numChildren": 1 }, "data": { "key": "NZXJBCMJ", "version": 1, "itemType": "journalArticle", "title": "Direct Regulation of Striated Muscle Myosins by Nitric Oxide and Endogenous Nitrosothiols", "creators": [ { "creatorType": "author", "firstName": "Alicia M.", "lastName": "Evangelista" }, { "creatorType": "author", "firstName": "Vijay S.", "lastName": "Rao" }, { "creatorType": "author", "firstName": "Ashley R.", "lastName": "Filo" }, { "creatorType": "author", "firstName": "Nadzeya V.", "lastName": "Marozkina" }, { "creatorType": "author", "firstName": "Allan", "lastName": "Doctor" }, { "creatorType": "author", "firstName": "David R.", "lastName": "Jones" }, { "creatorType": "author", "firstName": "Benjamin", "lastName": "Gaston" }, { "creatorType": "author", "firstName": "William H.", "lastName": "Guilford" } ], "abstractNote": "Nitric oxide (NO) has long been recognized to affect muscle contraction [1], both through activation of guanylyl cyclase and through modification of cysteines in proteins to yield S-nitrosothiols. While NO affects the contractile apparatus directly, the identities of the target myofibrillar proteins remain unknown. Here we report that nitrogen oxides directly regulate striated muscle myosins.\n\nExposure of skeletal and cardiac myosins to physiological concentrations of nitrogen oxides, including the endogenous nitrosothiol S-nitroso-L-cysteine, reduced the velocity of actin filaments over myosin in a dose-dependent and oxygen-dependent manner, caused a doubling of force as measured in a laser trap transducer, and caused S-nitrosylation of cysteines in the myosin heavy chain. These biomechanical effects were not observed in response to S-nitroso-D-cysteine, demonstrating specificity for the naturally occurring isomer. Both myosin heavy chain isoforms in rats and cardiac myosin heavy chain from human were S-nitrosylated in vivo.\n\nThese data show that nitrosylation signaling acts as a molecular “gear shift” for myosin—an altogether novel mechanism by which striated muscle and cellular biomechanics may be regulated.", "publicationTitle": "PLoS ONE", "publisher": "", "place": "", "date": "June 18, 2010", "volume": "5", "issue": "6", "section": "", "partNumber": "", "partTitle": "", "pages": "e11209", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "PLoS ONE", "DOI": "10.1371/journal.pone.0011209", "citationKey": "", "url": "http://dx.doi.org/10.1371/journal.pone.0011209", "accessDate": "2012-05-01T17:26:51Z", "PMID": "", "PMCID": "", "ISSN": "", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "PLoS ONE", "callNumber": "", "rights": "", "extra": "", "tags": [], "collections": [], "relations": {}, "dateAdded": "2012-05-01T17:26:51Z", "dateModified": "2012-05-01T17:26:51Z" } }, { "key": "C6JB3X3F", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/C6JB3X3F", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/C6JB3X3F", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/TW5N5T67", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } } }, "data": { "key": "C6JB3X3F", "version": 1, "parentItem": "TW5N5T67", "itemType": "attachment", "linkMode": "linked_url", "title": "Biochem. J. (2005) 389, 333-341 - E.M. Jimenez-Mateos and others - MAP1B can modify the LIS1-dynein interaction", "accessDate": "2012-05-01T16:16:46Z", "url": "http://www.biochemj.org/bj/389/0333/bj3890333.htm", "note": "", "contentType": "text/html", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T16:16:46Z", "dateModified": "2012-05-01T16:16:46Z" } }, { "key": "TW5N5T67", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/TW5N5T67", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/TW5N5T67", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } }, "creatorSummary": "JiméNez-Mateos et al.", "parsedDate": "2005-07-15", "numChildren": 1 }, "data": { "key": "TW5N5T67", "version": 1, "itemType": "journalArticle", "title": "Binding of microtubule-associated protein 1B to LIS1 affects the interaction between dynein and LIS1", "creators": [ { "creatorType": "author", "firstName": "Eva M.", "lastName": "JiméNez-Mateos" }, { "creatorType": "author", "firstName": "Francisco", "lastName": "Wandosell" }, { "creatorType": "author", "firstName": "Orly", "lastName": "Reiner" }, { "creatorType": "author", "firstName": "Jesús", "lastName": "Avila" }, { "creatorType": "author", "firstName": "Christian", "lastName": "González-Billault" } ], "abstractNote": "", "publicationTitle": "Biochemical Journal", "publisher": "", "place": "", "date": "2005-7-15", "volume": "389", "issue": "2", "section": "", "partNumber": "", "partTitle": "", "pages": "333", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "", "DOI": "10.1042/BJ20050244", "citationKey": "", "url": "http://www.biochemj.org/bj/389/0333/bj3890333.htm", "accessDate": "2012-05-01T16:16:46Z", "PMID": "", "PMCID": "", "ISSN": "02646021, 14708728", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "CrossRef", "callNumber": "", "rights": "", "extra": "", "tags": [], "collections": [], "relations": {}, "dateAdded": "2012-05-01T16:16:46Z", "dateModified": "2012-05-01T16:16:46Z" } }, { "key": "KIEJUAZ2", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/KIEJUAZ2", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/KIEJUAZ2", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/76IZUAN3", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } } }, "data": { "key": "KIEJUAZ2", "version": 1, "parentItem": "76IZUAN3", "itemType": "attachment", "linkMode": "linked_url", "title": "Full Text PDF", "accessDate": "2012-05-01T16:01:41Z", "url": "http://onlinelibrary.wiley.com/store/10.1111/j.1749-6632.2008.03998.x/asset/j.1749-6632.2008.03998.x.pdf?v=1&t=h1p5a792&s=9424eb9e075abeded906847ddafece6bbc345fc0", "note": "", "contentType": "application/pdf", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T16:01:41Z", "dateModified": "2012-05-01T16:01:41Z" } }, { "key": "75GB558T", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/75GB558T", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/75GB558T", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/76IZUAN3", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } } }, "data": { "key": "75GB558T", "version": 1, "parentItem": "76IZUAN3", "itemType": "attachment", "linkMode": "linked_url", "title": "Snapshot", "accessDate": "2012-05-01T16:01:41Z", "url": "http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2008.03998.x/abstract", "note": "", "contentType": "text/html", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T16:01:41Z", "dateModified": "2012-05-01T16:01:41Z" } }, { "key": "76IZUAN3", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/76IZUAN3", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/76IZUAN3", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } }, "creatorSummary": "Momboisse et al.", "parsedDate": "2009-01-21", "numChildren": 2 }, "data": { "key": "76IZUAN3", "version": 1, "itemType": "journalArticle", "title": "Calcium‐regulated Exocytosis in Neuroendocrine Cells: Intersectin‐1L Stimulates Actin Polymerization and Exocytosis by Activating Cdc42", "creators": [ { "creatorType": "author", "firstName": "Fanny", "lastName": "Momboisse" }, { "creatorType": "author", "firstName": "Stéphane", "lastName": "Ory" }, { "creatorType": "author", "firstName": "Valerie", "lastName": "Calco" }, { "creatorType": "author", "firstName": "Magali", "lastName": "Malacombe" }, { "creatorType": "author", "firstName": "Marie‐France", "lastName": "Bader" }, { "creatorType": "author", "firstName": "Stéphane", "lastName": "Gasman" } ], "abstractNote": "Actin cytoskeleton remodeling is a critical step of regulated exocytosis in many secretory cell types, including neuroendocrine cells. While the classical model considers the cortical actin network as a physical barrier preventing the uncontrolled recruitment of secretory granules to the plasma membrane docking sites, recent evidence supports the idea that actin polymerization also plays a more active role in the late stages of exocytosis. However, the molecular machinery underlying this positive function of actin in the course of exocytosis remains largely unknown. Here, we propose that the neuronal guanine nucleotide exchange factor, intersectin-1L, activates the GTPase Cdc42, which in turn provides de novo actin filaments that are important for calcium-regulated exocytosis in PC12 cells.", "publicationTitle": "Annals of the New York Academy of Sciences", "publisher": "", "place": "", "date": "2009/01/21", "volume": "1152", "issue": "1", "section": "", "partNumber": "", "partTitle": "", "pages": "209-214", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "", "DOI": "10.1111/j.1749-6632.2008.03998.x", "citationKey": "", "url": "http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2008.03998.x/abstract", "accessDate": "2012-05-01T16:01:41Z", "PMID": "", "PMCID": "", "ISSN": "1749-6632", "archive": "", "archiveLocation": "", "shortTitle": "Calcium‐regulated Exocytosis in Neuroendocrine Cells", "language": "en", "libraryCatalog": "onlinelibrary.wiley.com", "callNumber": "", "rights": "© 2009 New York Academy of Sciences", "extra": "", "tags": [ { "tag": "Cdc42", "type": 1 }, { "tag": "Exocytosis", "type": 1 }, { "tag": "PC12 Cells", "type": 1 }, { "tag": "actin", "type": 1 }, { "tag": "intersectin", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T16:01:41Z", "dateModified": "2012-05-01T16:01:41Z" } }, { "key": "44XZXVR7", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/44XZXVR7", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/44XZXVR7", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/WT5X6WFQ", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } } }, "data": { "key": "44XZXVR7", "version": 1, "parentItem": "WT5X6WFQ", "itemType": "attachment", "linkMode": "linked_url", "title": "Snapshot", "accessDate": "2012-05-01T06:12:09Z", "url": "http://stroke.ahajournals.org/content/28/6/1283.full", "note": "", "contentType": "text/html", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T06:12:09Z", "dateModified": "2012-05-01T06:12:09Z" } }, { "key": "WT5X6WFQ", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/WT5X6WFQ", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/WT5X6WFQ", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } }, "creatorSummary": "Samdani et al.", "parsedDate": "1997-06-01", "numChildren": 1 }, "data": { "key": "WT5X6WFQ", "version": 1, "itemType": "journalArticle", "title": "Nitric Oxide Synthase in Models of Focal Ischemia", "creators": [ { "creatorType": "author", "firstName": "Amer F", "lastName": "Samdani" }, { "creatorType": "author", "firstName": "Ted M", "lastName": "Dawson" }, { "creatorType": "author", "firstName": "Valina L", "lastName": "Dawson" } ], "abstractNote": "Background and Purpose Cessation of blood flow to the brain, for even a few minutes, sets in motion a potential reversible cascade of events resulting in neuronal cell death. Oxygen free radicals and oxidants appear to play an important role in central nervous system injury after cerebral ischemia and reperfusion. Recently, divergent roles for the newly identified neuronal messenger molecule and oxygen radical, nitric oxide (NO), have been identified in various models of cerebral ischemia. Because of the chemical and physical properties of NO, the numerous physiological activities it mediates, and the lack of specific agents to modulate the activity of the different isoforms of NO synthase (NOS), reports regarding the role of NO in focal cerebral ischemia have been confounding and often conflicting. Recent advances in pharmacology and the development of transgenic knockout mice specific for the different isoforms of NOS have advanced our knowledge and clarified the role of NO in cerebral ischemia.\nMethods Animal models of focal ischemia employ occlusion of nutrient cerebral vessels, most commonly the middle cerebral artery. Primary cortical cultures are exposed to excitotoxic or ischemic conditions, and the activities of NOS isoforms or NO production are evaluated. Transgenic mice lacking expression of either the neuronal isoform of NOS (nNOS), the endothelial isoform of NOS (eNOS), or the immunologic isoform of NOS (iNOS) have been examined in models of excitotoxic injury and ischemia.\nResults Excitotoxic or ischemic conditions excessively activate nNOS, resulting in concentrations of NO that are toxic to surrounding neurons. Conversely, NO generated from eNOS is critical in maintaining cerebral blood flow and reducing infarct volume. iNOS, which is not normally present in healthy tissue, is induced shortly after ischemia and contributes to secondary late-phase damage.\nConclusions Pharmacological and genetic approaches have significantly advanced our knowledge regarding the role of NO and the different NOS isoforms in focal cerebral ischemia. nNOS and iNOS play key roles in neurodegeneration, while eNOS plays a prominent role in maintaining cerebral blood flow and preventing neuronal injury.", "publicationTitle": "Stroke", "publisher": "", "place": "", "date": "06/01/1997", "volume": "28", "issue": "6", "section": "", "partNumber": "", "partTitle": "", "pages": "1283-1288", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Stroke", "DOI": "10.1161/01.STR.28.6.1283", "citationKey": "", "url": "http://stroke.ahajournals.org/content/28/6/1283", "accessDate": "2012-05-01T06:12:09Z", "PMID": "", "PMCID": "", "ISSN": "0039-2499, 1524-4628", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "en", "libraryCatalog": "stroke.ahajournals.org", "callNumber": "", "rights": "", "extra": "", "tags": [], "collections": [], "relations": {}, "dateAdded": "2012-05-01T06:12:09Z", "dateModified": "2012-05-01T06:12:09Z" } }, { "key": "TA2TTDWQ", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/TA2TTDWQ", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/TA2TTDWQ", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } }, "creatorSummary": "Ji et al.", "parsedDate": "1999-02-01", "numChildren": 0 }, "data": { "key": "TA2TTDWQ", "version": 1, "itemType": "journalArticle", "title": "S-nitrosylation and S-glutathiolation of protein sulfhydryls by S-nitroso glutathione", "creators": [ { "creatorType": "author", "firstName": "Y", "lastName": "Ji" }, { "creatorType": "author", "firstName": "T P", "lastName": "Akerboom" }, { "creatorType": "author", "firstName": "H", "lastName": "Sies" }, { "creatorType": "author", "firstName": "J A", "lastName": "Thomas" } ], "abstractNote": "The modification of reactive protein sulfhydryls by S-nitrosoglutathione and other NO donors has been studied by gel isoelectric focusing. S-nitrosylated, unmodified, and S-glutathiolated protein forms are differentiated by this method. With specific antibodies for the protein of interest, both S-nitrosylation and S-glutathiolation of the protein were analyzed in mixtures obtained as soluble tissue or cell extracts. The effect of S-nitrosoglutathione (GSNO) on purified phosphorylase b, on carbonic anhydrase III in an extract from rat liver, and on H-ras expressed in Escherichia coli was examined. When fresh GSNO reacted with pure phosphorylase b, only S-nitrosylated forms of the protein were observed. Likewise the NO donors, amyl nitrite, spermine NONOate, and diethylamine NONOate, all generated S-nitrosylated phosphorylase b. When crude mixtures of proteins from rat liver (containing carbonic anhydrase III) or from E. coli (containing an overexpressed form of H-ras) were exposed to fresh GSNO, both the S-nitrosylated and the S-glutathiolated forms of the proteins were observed. It is suggested that reactive intermediates from the breakdown of GSNO are responsible for the observed S-glutathiolation. These experiments show that both S-nitrosylated and S-glutathiolated forms of proteins may be generated by the addition of GSNO to mixtures containing proteins with reactive sulfhydryls. These protein modifications may exhibit metabolic consequences independent of the release of nitric oxide.", "publicationTitle": "Archives of Biochemistry and Biophysics", "publisher": "", "place": "", "date": "Feb 1, 1999", "volume": "362", "issue": "1", "section": "", "partNumber": "", "partTitle": "", "pages": "67-78", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Arch. Biochem. Biophys.", "DOI": "10.1006/abbi.1998.1013", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/9917330", "accessDate": "2012-05-01T04:17:34Z", "PMID": "", "PMCID": "", "ISSN": "0003-9861", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 9917330", "tags": [ { "tag": "Animals", "type": 1 }, { "tag": "Enzyme Stability", "type": 1 }, { "tag": "Glutathione", "type": 1 }, { "tag": "Isoelectric Focusing", "type": 1 }, { "tag": "Male", "type": 1 }, { "tag": "Nitroso Compounds", "type": 1 }, { "tag": "Phosphorylase b", "type": 1 }, { "tag": "Proteins", "type": 1 }, { "tag": "Rabbits", "type": 1 }, { "tag": "Rats", "type": 1 }, { "tag": "Rats, Sprague-Dawley", "type": 1 }, { "tag": "S-Nitrosoglutathione", "type": 1 }, { "tag": "Sulfhydryl Compounds", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2012-05-01T04:17:34Z", "dateModified": "2012-05-01T04:17:34Z" } }, { "key": "JNG9TIW8", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/JNG9TIW8", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/JNG9TIW8", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/ZZ76P96E", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } } }, "data": { "key": "JNG9TIW8", "version": 1, "parentItem": "ZZ76P96E", "itemType": "attachment", "linkMode": "linked_url", "title": "Full Text PDF", "accessDate": "2012-05-01T03:52:16Z", "url": "http://onlinelibrary.wiley.com/store/10.1002/art.1780391118/asset/1780391118_ftp.pdf?v=1&t=h1of87g4&s=7bffa050d26ca46b715a00c1931e1c9a3d88af17", "note": "", "contentType": "application/pdf", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T03:52:16Z", "dateModified": "2012-05-01T03:52:16Z" } }, { "key": "ICQVZKWZ", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/ICQVZKWZ", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/ICQVZKWZ", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/69386/items/ZZ76P96E", "type": "application/json" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } } }, "data": { "key": "ICQVZKWZ", "version": 1, "parentItem": "ZZ76P96E", "itemType": "attachment", "linkMode": "linked_url", "title": "Snapshot", "accessDate": "2012-05-01T03:52:16Z", "url": "http://onlinelibrary.wiley.com/doi/10.1002/art.1780391118/abstract", "note": "", "contentType": "text/html", "charset": "", "tags": [], "relations": {}, "dateAdded": "2012-05-01T03:52:16Z", "dateModified": "2012-05-01T03:52:16Z" } }, { "key": "ZZ76P96E", "version": 1, "library": { "type": "group", "id": 69386, "name": "Team Nitrosylplatz", "links": { "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/69386/items/ZZ76P96E", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/team_nitrosylplatz/items/ZZ76P96E", "type": "text/html" } }, "meta": { "createdByUser": { "id": 900824, "username": "Matt_Jenny", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/matt_jenny", "type": "text/html" } } }, "creatorSummary": "Frenkel et al.", "parsedDate": "2005-12-12", "numChildren": 2 }, "data": { "key": "ZZ76P96E", "version": 1, "itemType": "journalArticle", "title": "Effects of nitric oxide on chondrocyte migration, adhesion, and cytoskeletal assembly", "creators": [ { "creatorType": "author", "firstName": "Sally R", "lastName": "Frenkel" }, { "creatorType": "author", "firstName": "Robert M", "lastName": "Clancy" }, { "creatorType": "author", "firstName": "John L", "lastName": "Ricci" }, { "creatorType": "author", "firstName": "Di", "lastName": "Cesare" }, { "creatorType": "author", "firstName": "Paul", "lastName": "E" }, { "creatorType": "author", "firstName": "John J", "lastName": "Rediske" }, { "creatorType": "author", "firstName": "Steven B", "lastName": "Abramson" } ], "abstractNote": "Objective. The migration of cells of chondrocyte lineage is believed to play a role in cartilage growth and repair. The present study examined 1) whether chondrocytes are capable of migration in vitro; and 2) the effects of nitric oxide (NO) on chondrocyte migration, adhesion, and cytoskeletal assembly.\nMethods. Chondrocyte migration was evaluated by 2 assays: 1) “centrifugal” migration within a 3-dimensional collagen matrix (dot culture); and 2) directed migration under agarose in response to bone morphogenetic protein. To assess the effects of NO, chondrocytes were treated with either exogenous NO (S-nitrosoglutathione [SNO-GSH]) or a mixture of cytokines known to induce endogenous NO production. The effects of NO on chondrocyte adhesion to fibronectin-coated surfaces, as well as on actin polymerization (determined by indirect immunofluorescence), were also examined.\nResults. The capacity of chondrocytes to migrate was demonstrated both by the dot culture and by agarose methods. Both SNO-GSH and endogenous NO induced by cytokines inhibited this migration. Exposure to NO also inhibited attachment of chondrocytes to fibronectin and disrupted assembly of actin filaments. These effects of SNO-GSH and cytokine-induced NO production were reversed in the presence of hemoglobin and the NO synthase inhibitor NG-monomethyl arginine, respectively.\nConclusion. NO interferes with chondrocyte migration and attachment to fibronectin, an extracellular matrix protein, probably via effects on the actin cytoskeleton. These effects of NO may result in impairment of cartilage repair, by interfering with the extracellular matrix regulation of chondrocyte function.", "publicationTitle": "Arthritis & Rheumatism", "publisher": "", "place": "", "date": "2005/12/12", "volume": "39", "issue": "11", "section": "", "partNumber": "", "partTitle": "", "pages": "1905-1912", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "", "DOI": "10.1002/art.1780391118", "citationKey": "", "url": "http://onlinelibrary.wiley.com/doi/10.1002/art.1780391118/abstract", "accessDate": "2012-05-01T03:52:16Z", "PMID": "", "PMCID": "", "ISSN": "1529-0131", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "en", "libraryCatalog": "onlinelibrary.wiley.com", "callNumber": "", "rights": "Copyright © 1996 American College of Rheumatology", "extra": "", "tags": [], "collections": [], "relations": {}, "dateAdded": "2012-05-01T03:52:16Z", "dateModified": "2012-05-01T03:52:16Z" } } ]