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ABSTRACT: Background
Activated fibroblasts (myofibroblasts) play a critical role in cardiac fibrosis; however, their origin in the diseased heart remains unclear, warranting further investigation. Recent studies suggest the contribution of bone marrow fibroblast progenitor cells (BM-FPCs) in pressure overload-induced cardiac fibrosis. We have previously shown that interleukin-10 (IL10) suppresses pressure overload-induced cardiac fibrosis; however, the role of IL10 in inhibition of BM-FPC-mediated cardiac fibrosis is not known. We hypothesized that IL10 inhibits pressure overload-induced homing of BM-FPCs to the heart and their transdifferentiation to myofibroblasts and thus attenuates cardiac fibrosis.Methods
Pressure overload was induced in wild-type (WT) and IL10 knockout (IL10KO)
SUBMITTER: Verma SK
PROVIDER: S-EPMC5736130 | biostudies-literature | 2017 Sep
REPOSITORIES: biostudies-literature