Genetic beta-catenin depletion significantly improved 4-week left ventricular fractional shortening (30.2% vs 24.0%, P<0.001) following experimental infarct in mice.
Beta-catenin depletion attenuates postinfarct left ventricular remodeling by enhancing the differentiation of resident cardiac progenitor cells.
Absolute Event Rate: 30.2% vs 24%
p-value: p=< 0.001
We analyzed the effect of conditional, alphaMHC-dependent genetic beta-catenin depletion and stabilization on cardiac remodeling following experimental infarct. beta-Catenin depletion significantly improved 4-week survival and left ventricular (LV) function (fractional shortening: CT(Deltaex3-6): 24 +/- 1.9%; beta-cat(Deltaex3-6): 30.2 +/- 1.6%, P 95%) Sca-1(pos) cardiac precursor cells from beta-catenin-depleted mice compared to cells isolated from control littermate demonstrated increased differentiation toward alpha-actin(pos) and cTnT(pos) cardiomyocytes after 10 days (CT(Deltaex3-6): 38.0 +/- 1.0% alpha-actin(pos); beta-cat(Deltaex3-6): 49.9 +/- 2.4% alpha-actin(pos), P < 0.001). We conclude that beta-catenin depletion attenuates postinfarct LV remodeling in part through increased differentiation of GATA4(pos)/Sca-1(pos) resident cardiac progenitor cells.
Zelarayán et al. (2008) studied Experimental infarct / cardiac remodeling. Conditional, alphaMHC-dependent genetic beta-catenin depletion vs. Control littermates was evaluated on Left ventricular fractional shortening at 4 weeks (p=< 0.001). Genetic beta-catenin depletion significantly improved 4-week left ventricular fractional shortening (30.2% vs 24.0%, P<0.001) following experimental infarct in mice.