Abstract
In a recent issue of Circulation, Verma et al. (1) uncover a new interleukin-10 (IL-10)-dependent mechanism inhibiting fibrosis in pressure overloaded mouse myocardium. In this study, pressure overload was achieved in wild-type (WT) and IL-10 knockout (IL-10KO) mice by transverse aortic constriction (TAC), a widely used experimental mouse model that creates pressure overload-induced left ventricular hypertrophy, leading to heart failure. IL-10KO mice displayed more bone marrow (BM)-derived fibroblast progenitor cell mobilization and homing to the heart. Chimeric IL-10KO mice with WT BM were protected against TAC-induced cardiac fibrosis and presented improved heart function. Verma et al. (1) found out that IL-10 inhibits homing and trans-differentiation of BM-derived fibroblast progenitor cells (FPC) in myofibroblasts, major effector cells of cardiac fibrosis. In vitro experiments performed on FPC isolated from mouse BM (prominin 1+ CD45+ cells) indicated that IL-10 could suppress the expression of the fibrosis-associated miR-21 in response to transforming growth factor-β (TGF-)β.
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