ZAK induces MMP-2 activity via JNK/p38 signals and reduces MMP-9 activity by increasing TIMP-1/2 expression in H9c2 cardiomyoblast cells.

doi:10.1007/s11010-008-0021-1.

中山醫學大學機構典藏 CSMUIR > 口腔醫學院 > 口腔醫學研究所 > 期刊論文 > Item 310902500/15667

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题名:	ZAK induces MMP-2 activity via JNK/p38 signals and reduces MMP-9 activity by increasing TIMP-1/2 expression in H9c2 cardiomyoblast cells.
作者:	YC1, Cheng WW, Kuo HC, Wu TY, Lai CH, Wu JM, Hwang WH, Wang FJ, Tsai JJ, Yang CY, Huang CH, Chu
贡献者:	中山醫大口腔科學研究所
日期:	2009-05
上传时间:	2016-08-09T03:41:43Z (UTC)
ISSN:	1573-4919
摘要:	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.
URI:	http://dx.doi.org/10.1007/s11010-008-0021-1 https://ir.csmu.edu.tw:8080/ir/handle/310902500/15667
關聯:	Mol Cell Biochem. 2009 May;325(1-2):69-77.
显示于类别:	[口腔醫學研究所] 期刊論文

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