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有读书笔记有附件Absence of SPARC results in increased cardiac rupture and dysfunction after acute myocardial infarction

宇晟 添加于 2010-6-1 12:01 | 2438 次阅读 | 0 个评论

  •  作 者

    Schellings MWM, Vanhoutte D, Swinnen M, Cleutjens JP, Debets J, van Leeuwen REW, d'Hooge J, Van de Werf F, Carmeliet P, Pinto YM, Sage EH, Heymans S

  •  摘 要

    The matricellular protein SPARC (secreted protein, acidic and rich in cysteine, also known as osteonectin) mediates cell-matrix interactions during wound healing and regulates the production and/or assembly of the extracellular matrix (ECM). This study investigated whether SPARC functions in infarct healing and ECM maturation after myocardial infarction (MI). In comparison with wild-type (WT) mice, animals with a targeted inactivation of SPARC exhibited a fourfold increase in mortality that resulted from an increased incidence of cardiac rupture and failure after MI. SPARC-null infarcts had a disorganized granulation tissue and immature collagenous ECM. In contrast, adenoviral overexpression of SPARC in WT mice improved the collagen maturation and prevented cardiac dilatation and dysfunction after MI. In cardiac fibroblasts in vitro, reduction of SPARC by short hairpin RNA attenuated transforming growth factor beta (TGF)-mediated increase of Smad2 phosphorylation, whereas addition of recombinant SPARC increased Smad2 phosphorylation concordant with increased Smad2 phosphorylation in SPARC-treated mice. Importantly, infusion of TGF-beta rescued cardiac rupture in SPARC-null mice but did not significantly alter infarct healing in WT mice. These findings indicate that local production of SPARC is essential for maintenance of the integrity of cardiac ECM after MI. The protective effects of SPARC emphasize the potential therapeutic applications of this protein to prevent cardiac dilatation and dysfunction after MI.

  •  详细资料

    • 关键词: Animals; Calcium-Binding Proteins/genetics; Extracellular Matrix Proteins/genetics; Female; Fibroblasts/drug effects/metabolism; Granulation Tissue/drug effects/metabolism/pathology; Heart/physiopathology; Heart Rupture, Post-Infarction/*metabolism/physiopathology/prevention & control; Hemodynamics/physiology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Myocardial Infarction/*metabolism/pathology/physiopathology; Myocardium/metabolism/pathology; Osteonectin/*deficiency/genetics/physiolog
    • 文献种类:期刊
    • 期刊名称: The Journal of Experimental Medicine
    • 期刊缩写: J Exp Med
    • 期卷页: 2009年  第206卷 第1期 113-123页
    • 地址: Center for Heart Failure Research, Cardiovascular Research Institute Maastricht, University Hospital Maastricht, 6229 HX Maastricht, The Netherlands
    • ISBN: 0022-1007
    • 备注:PMID:19103879

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  •  附 件

    PDF附件Absence of SPARC results in increased cardiac rupture and dysfunction after acute myocardial infarction 

  •  宇晟 的文献笔记  订阅

    a good paper about sparc investigation IF：15.64
    In my opinion, this paper provide a good strategy we can follow.It combined in vivo experiment and in vitro, containing konck out ,silencing and overexpression .Moreover, it related to potential mechanism.This paper is attached.
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