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    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/15667

    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: YC1, Cheng
    WW, Kuo
    HC, Wu
    TY, Lai
    CH, Wu
    JM, Hwang
    WH, Wang
    FJ, Tsai
    JJ, Yang
    CY, Huang
    CH, Chu
    Contributors: 中山醫大口腔科學研究所
    Date: 2009-05
    Issue Date: 2016-08-09T03:41:43Z (UTC)
    ISSN: 1573-4919
    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.
    URI: http://dx.doi.org/10.1007/s11010-008-0021-1
    Relation: Mol Cell Biochem. 2009 May;325(1-2):69-77.
    Appears in Collections:[口腔醫學研究所] 期刊論文

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