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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0017262,
umls-concept:C0145947,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0392756,
umls-concept:C1150182,
umls-concept:C1150183,
umls-concept:C1150587,
umls-concept:C1366876,
umls-concept:C1367731,
umls-concept:C1705632,
umls-concept:C1710082,
umls-concept:C1833235,
umls-concept:C1868689,
umls-concept:C2911684
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pubmed:issue |
1-2
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pubmed:dateCreated |
2009-4-1
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pubmed:abstractText |
Leucine-zipper and sterile-alpha motif kinase (ZAK) is the key intra-cellular mediator protein in cardiomyocyte hypertrophy induction by transforming growth factor beta 1 (TGF-beta1) which has also been identified as a profibrotic cytokine involved in cardiac fibrosis progression. We hypothesized whether ZAK over-expression causes cardiac scar formation due to the extra-cellular matrix (ECM) degraded enzyme regulation in this paper. Using immuno-histochemical analysis of the human cardiovascular tissue array, we found a positively significant association between ZAK over-expression and myocardial scars. ZAK over-expression in H9c2 cardiomyoblast cells increases the metalloproteinase tissue inhibitor 1/2 (TIMP-1/2) protein level, which reduces matria metalloproteinase-9 (MMP-9) activity and also activates c-JNK N-terminal kinase 1/2 (JNK1/2) and p38 signaling, which induces MMP-2, possibly resulting in cardiac fibrosis. Taken together, ZAK activity inhibition may be a good strategy to prevent the cardiac fibrosis progression.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1573-4919
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pubmed:author |
pubmed-author:ChengYi-ChangYC,
pubmed-author:ChuChun-HsienCH,
pubmed-author:HuangChih-YangCY,
pubmed-author:HwangJin-MingJM,
pubmed-author:KuoWei-WenWW,
pubmed-author:LaiTung-YuanTY,
pubmed-author:TsaiFuu-JenFJ,
pubmed-author:WangWen-HongWH,
pubmed-author:WuChun-HsienCH,
pubmed-author:WuHsi-ChinHC,
pubmed-author:YangJaw-JiJJ
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pubmed:issnType |
Electronic
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pubmed:volume |
325
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
69-77
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:19184368-Animals,
pubmed-meshheading:19184368-Cell Line,
pubmed-meshheading:19184368-Immunohistochemistry,
pubmed-meshheading:19184368-MAP Kinase Signaling System,
pubmed-meshheading:19184368-Matrix Metalloproteinase 2,
pubmed-meshheading:19184368-Matrix Metalloproteinase 9,
pubmed-meshheading:19184368-Myocardium,
pubmed-meshheading:19184368-Protein Kinases,
pubmed-meshheading:19184368-Rats,
pubmed-meshheading:19184368-Signal Transduction,
pubmed-meshheading:19184368-Tissue Inhibitor of Metalloproteinase-1,
pubmed-meshheading:19184368-Tissue Inhibitor of Metalloproteinase-2,
pubmed-meshheading:19184368-p38 Mitogen-Activated Protein Kinases
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pubmed:year |
2009
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pubmed:articleTitle |
ZAK induces MMP-2 activity via JNK/p38 signals and reduces MMP-9 activity by increasing TIMP-1/2 expression in H9c2 cardiomyoblast cells.
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pubmed:affiliation |
Emergency Department, China Medical University Hospital, Taichung, Taiwan.
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pubmed:publicationType |
Journal Article
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