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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16303


    Title: ZAK induces MMP-2 activity via JNK/ p38 signals and reduces MMP-9 activity by increasing TIMP-1/2 expression in H9c2 cardiomyoblast cells
    Authors: ;Cheng, Yi-Chang;Kuo, Wei-Wen;Wu, Hsi-Chin;Lai, ung-Yuan;Hwang, Jin-Ming;Wang, Wen-Hung;Tsai, Fuu-Jen;Yang, Jaw-Ji;黃志揚;HUANG, CHIH-YANG;Chu, Chun-Hsien
    Contributors: 生物科技學系
    Date: 2009-01
    Issue Date: 2012-11-23 17:11:13 (UTC+8)
    Abstract: 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.
    Relation: MOLECULAR AND CELLULAR BIOCHEMISTRY; 325(1-2):69-77.
    Appears in Collections:[生物科技學系] 期刊論文

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