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    J Renin Angiotensin Aldosterone Syst. 2012 Mar;13(1):67-75. Epub 2011 Oct 21.

    Angiotensin II induces extracellular matrix metalloproteinase inducer expression via an AT1R dependent pathway in aortic atherosclerotic plaque in apolipoprotein E knockout mice.

    Source

    Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan, China. doctorlxyang@163.com

    Abstract

    The pathogenesis of acute coronary syndrome is rupture of vulnerable plaque. Extracellular matrix metalloproteinase inducer (EMMPRIN) is reported to have a important role in the destabilization of atheroma.

    OBJECTIVES:

    this investigation examined the effect of angiotensin II (Ang II) on EMMPRIN expression in atherosclerotic plaques in ApoE knockout mice.

    METHODS:

    ApoE knockout mice were fed a high fat diet to establish an atherosclerosis model then intervention was made with Ang II and valsartan. EMMPRIN gene and its protein expression were measured by real-time PCR immunohistochemistry, and Western blot.

    RESULTS:

    EMMPRIN gene and protein expression intervened with Ang II were significantly increased; valsartan could inhibit the effect of Ang II.

    CONCLUSION:

    Ang II up-regulated EMMPRIN expression in atherosclerotic plaque via AT1R, and valsartan could inhibit the effect of Ang II.

    PMID:
    22020146
    [PubMed - in process]

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