| pubmed-article:11179198 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11179198 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:11179198 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:11179198 | lifeskim:mentions | umls-concept:C0524828 | lld:lifeskim |
| pubmed-article:11179198 | lifeskim:mentions | umls-concept:C0872053 | lld:lifeskim |
| pubmed-article:11179198 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:11179198 | pubmed:dateCreated | 2001-2-22 | lld:pubmed |
| pubmed-article:11179198 | pubmed:abstractText | Nitric oxide (NO) induces apoptosis in cardiac myocytes through an oxidant-sensitive mechanism. However, additional factors appear to modulate the exact timing and rate of NO-dependent apoptosis. In this study, we investigated the role of mitogen-activated protein kinases (MAPKs) (extracellular signal-regulated kinase [ERK] 1/2, c-Jun N-terminal kinase [JNK] 1/2, and p38MAPK) in NO-mediated apoptotic signaling. The NO donor S:-nitrosoglutathione (GSNO) induced caspase-dependent apoptosis in neonatal rat cardiac myocytes, preceded by a rapid (<10-minute) and significant (approximately 50-fold) activation of JNK1/2. Activation of JNK was cGMP dependent and was inversely related to NO concentration; it was maximal at the lowest dose of GSNO (10 micromol/L) and negligible at 1 mmol/L. NO slightly increased ERK1/2 beginning at 2 hours but did not affect p38MAPK activity. Inhibitors of ERK and p38MAPK activation did not affect cell death rates. In contrast, expression of dominant-negative JNK1 or MKK4 mutants significantly increased NO-induced apoptosis at 5 hours (56.77% and 57.37%, respectively, versus control, 40.5%), whereas MEKK1, an upstream activator of JNK, sharply reduced apoptosis in a JNK-dependent manner. Adenovirus-mediated expression of dominant-negative JNK1 both eliminated the rapid activation of JNK by NO and accelerated NO-mediated apoptosis by approximately 2 hours. These data indicate that NO activates JNK as part of a cytoprotective response, concurrent with initiation of apoptotic signaling. Early, transient activation of JNK serves both to delay and to reduce the total extent of apoptosis in cardiac myocytes. | lld:pubmed |
| pubmed-article:11179198 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11179198 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11179198 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11179198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11179198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11179198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11179198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11179198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11179198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11179198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11179198 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11179198 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:11179198 | pubmed:issn | 1524-4571 | lld:pubmed |
| pubmed-article:11179198 | pubmed:author | pubmed-author:BishopricN... | lld:pubmed |
| pubmed-article:11179198 | pubmed:author | pubmed-author:WebsterK AKA | lld:pubmed |
| pubmed-article:11179198 | pubmed:author | pubmed-author:DoughertyCC | lld:pubmed |
| pubmed-article:11179198 | pubmed:author | pubmed-author:ZannMM | lld:pubmed |
| pubmed-article:11179198 | pubmed:author | pubmed-author:SlepakT ITI | lld:pubmed |
| pubmed-article:11179198 | pubmed:author | pubmed-author:AndrekaPP | lld:pubmed |
| pubmed-article:11179198 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:11179198 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:11179198 | pubmed:volume | 88 | lld:pubmed |
| pubmed-article:11179198 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11179198 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11179198 | pubmed:pagination | 305-12 | lld:pubmed |
| pubmed-article:11179198 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11179198 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11179198 | pubmed:articleTitle | Cytoprotection by Jun kinase during nitric oxide-induced cardiac myocyte apoptosis. | lld:pubmed |
| pubmed-article:11179198 | pubmed:affiliation | Department of Molecular and Cellular Pharmacology, University of Miami, FL, USA. | lld:pubmed |
| pubmed-article:11179198 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11179198 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11179198 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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