DC Field | Value | Language |
---|---|---|
dc.contributor.author | Oh, Young-Bin | ko |
dc.contributor.author | Ahn, Min | ko |
dc.contributor.author | Lee, Sang-Myeong | ko |
dc.contributor.author | Koh, Hyoung-Won | ko |
dc.contributor.author | Lee, Sun-Hwa | ko |
dc.contributor.author | Kim, Suhn Hee | ko |
dc.contributor.author | Park, Byung-Hyun | ko |
dc.date.accessioned | 2024-03-22T07:02:37Z | - |
dc.date.available | 2024-03-22T07:02:37Z | - |
dc.date.created | 2024-03-21 | - |
dc.date.created | 2024-03-21 | - |
dc.date.issued | 2013-05 | - |
dc.identifier.citation | EXPERIMENTAL AND MOLECULAR MEDICINE, v.45 | - |
dc.identifier.issn | 1226-3613 | - |
dc.identifier.uri | http://hdl.handle.net/10203/318801 | - |
dc.description.abstract | Recent studies have documented that Janus-activated kinase (JAK)-signal transducer and activator of transcription (STAT) pathway can modulate the apoptotic program in a myocardial ischemia/reperfusion (I/R) model. To date, however, limited studies have examined the role of JAK3 on myocardial I/R injury. Here, we investigated the potential effects of pharmacological JAK3 inhibition with JANEX-1 in a myocardial I/R model. Mice were subjected to 45 min of ischemia followed by varying periods of reperfusion. JANEX-1 was injected 1 h before ischemia by intraperitoneal injection. Treatment with JANEX-1 significantly decreased plasma creatine kinase and lactate dehydrogenase activities, reduced infarct size, reversed I/R-induced functional deterioration of the myocardium and reduced myocardial apoptosis. Histological analysis revealed an increase in neutrophil and macrophage infiltration within the infarcted area, which was markedly reduced by JANEX-1 treatment. In parallel, in in vitro studies where neutrophils and macrophages were treated with JANEX-1 or isolated from JAK3 knockout mice, there was an impairment in the migration potential toward interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1), respectively. Of note, however, JANEX-1 did not affect the expression of IL-8 and MCP-1 in the myocardium. The pharmacological inhibition of JAK3 might represent an effective approach to reduce inflammation-mediated apoptotic damage initiated by myocardial I/R injury. | - |
dc.language | English | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.title | Inhibition of Janus activated kinase-3 protects against myocardial ischemia and reperfusion injury in mice | - |
dc.type | Article | - |
dc.identifier.wosid | 000321185200003 | - |
dc.identifier.scopusid | 2-s2.0-84881170395 | - |
dc.type.rims | ART | - |
dc.citation.volume | 45 | - |
dc.citation.publicationname | EXPERIMENTAL AND MOLECULAR MEDICINE | - |
dc.identifier.doi | 10.1038/emm.2013.43 | - |
dc.contributor.localauthor | Park, Byung-Hyun | - |
dc.contributor.nonIdAuthor | Oh, Young-Bin | - |
dc.contributor.nonIdAuthor | Ahn, Min | - |
dc.contributor.nonIdAuthor | Lee, Sang-Myeong | - |
dc.contributor.nonIdAuthor | Koh, Hyoung-Won | - |
dc.contributor.nonIdAuthor | Lee, Sun-Hwa | - |
dc.contributor.nonIdAuthor | Kim, Suhn Hee | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | infiltration | - |
dc.subject.keywordAuthor | ischemia/reperfusion | - |
dc.subject.keywordAuthor | JAK3 | - |
dc.subject.keywordAuthor | JANEX-1 | - |
dc.subject.keywordPlus | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | - |
dc.subject.keywordPlus | JAK/STAT PATHWAY | - |
dc.subject.keywordPlus | INFLAMMATORY RESPONSE | - |
dc.subject.keywordPlus | CANINE MYOCARDIUM | - |
dc.subject.keywordPlus | INFARCT SIZE | - |
dc.subject.keywordPlus | JAK3 | - |
dc.subject.keywordPlus | PREVENTION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | PATHOGENESIS | - |
dc.subject.keywordPlus | INDUCTION | - |
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