Key result
Infusion of c-kit(+) resident cardiac stem cells post-TAC increased RCSC density two-fold and markedly reduced myocardial fibrosis, apoptosis, and oxidative stress.
Why the study?
Does intravenous infusion of c-kit(+) resident cardiac stem cells reduce myocardial fibrosis in mice subjected to pressure overload?
Does intravenous infusion of c-kit(+) resident cardiac stem cells reduce myocardial fibrosis in mice subjected to pressure overload?
Intravenous infusion of c-kit(+) resident cardiac stem cells reduces myocardial fibrosis and improves remodeling in a mouse model of pressure overload.
Should not change clinical practice; hypothesis-generating for c-kit+ stem cells in pressure-overload remodeling.
To investigate the effect of resident cardiac stem cells (RCSC) on myocardial remodeling, c-kit(+) RCSC were isolated from hearts of C57Bl/6-Tg (ACTb-EGFP)1Osb/J mice expressing green fluorescent protein and expanded in vitro. C57/Bl6N wildtype mice were subjected to transverse aortic constriction (TAC, 360 μm) or sham-operation. 5 × 10(5) c-kit(+) RCSC or c-kit(-) cardiac cells or cell buffer were infused intravenously 24 h post-surgery (n = 11-24 per group). Hypoxia-inducible factor-1α-mRNA in left ventricles of TAC mice was enhanced 24 h after transplantation. 35 days post-TAC, the density of c-kit(+) RCSC in the myocardium was increased by two-fold. Infusion of c-kit(+) resident cardiac stem cells post-TAC markedly reduced myocardial fibrosis and the expression of collagen Iα2 and connective tissue growth factor. Infusion of c-kit(-) cardiac cells did not ameliorate cardiac fibrosis. In parallel, expression of pro-angiogenic mediators (FGFb, IL-4, IL-6, TGFß, leptin) and the density of CD31(+) and CD31(+) GFP(+) endothelial cells were increased. Transplantation reduced brain- and atrial natriuretic peptides and the cardiomyocyte cross-sectional area. Infusion of c-kit(+) resident cardiac stem reduced the rate of apoptosis and oxidative stress in cardiomyocytes and in non-cardiomyocyte cells.
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Kazakov et al. (2015) studied Pressure overload / myocardial remodeling. c-kit(+) resident cardiac stem cells vs. c-kit(-) cardiac cells or cell buffer was evaluated on Myocardial fibrosis and expression of collagen Iα2 and connective tissue growth factor. Infusion of c-kit(+) resident cardiac stem cells post-TAC increased RCSC density two-fold and markedly reduced myocardial fibrosis, apoptosis, and oxidative stress.
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