Reduction of Infarct Size and Prevention of Cardiac Rupture in Transgenic Mice Overexpressing FrzA
Circulation. 2003-11-04; 108(18): 2282-2289
DOI: 10.1161/01.CIR.0000093186.22847.4C
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1. Circulation. 2003 Nov 4;108(18):2282-9. Epub 2003 Oct 27.
Reduction of infarct size and prevention of cardiac rupture in transgenic mice
overexpressing FrzA.
Barandon L(1), Couffinhal T, Ezan J, Dufourcq P, Costet P, Alzieu P, Leroux L,
Moreau C, Dare D, Duplàa C.
Author information:
(1)Department of Cardiovascular Surgery and Cardiology, Hôpital Haut Lévêque,
Pessac, France.
BACKGROUND: FrzA/sFRP-1, a secreted, frizzled-related protein and antagonist for
the wnt/frizzled pathway, is expressed in the heart and vessels during mouse
embryogenesis and adulthood. FrzA is involved in cell cycle control of vascular
cells and angiogenesis. We assessed the hypothesis that FrzA could control the
healing process after myocardial infarction (MI).
METHODS AND RESULTS: We demonstrated an upregulation of sFRP-1 and distinct wnt
and fz member expression after MI. We established transgenic (Tg) mice that
overexpress FrzA under a cytomegalovirus promoter and developed a model of MI by
coronary artery ligation. FrzA reduced cardiac rupture after MI in Tg (6.5%
versus 26.4% in controls; n=165, P