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Transforming growth factor-β1 (TGF-β1) is a potent inducer of fibroblast to myofibroblast differentiation and contributes to the pro-fibrotic microenvironment during cardiac remodeling. Fibroblast growth factor-2 (FGF-2) is a growth factor secreted by adipose tissue-derived stromal cells (ASC) which can antagonize TGF-β1 signaling. We hypothesized that TGF-β1-induced cardiac fibroblast to myofibroblast differentiation is abrogated by FGF-2 and ASC conditioned medium (ASC-CMed). Our experiments demonstrated that TGF-β1 treatment-induced cardiac fibroblast differentiation into myofibroblasts, as evidenced by the formation of contractile stress fibers rich in αSMA. FGF-2 blocked the differentiation, as evidenced by the reduction in gene ( TAGLN , p < 0.0001;  ACTA2 , p = 0.0056) and protein (αSMA, p = 0.0338) expression of mesenchymal markers and extracellular matrix components gene expression ( COL1A1 , p < 0.0001;  COL3A1 , p = 0.0029). ASC-CMed did not block myofibroblast differentiation. The treatment with FGF-2 increased matrix metalloproteinases gene expression ( MMP1 , p < 0.0001;  MMP14 , p = 0.0027) and decreased the expression of tissue inhibitor of metalloproteinase gene  TIMP2  (p = 0.0023). ASC-CMed did not influence these genes. The proliferation of TGF-β1-induced human cardiac fibroblasts was restored by both FGF-2 (p = 0.0002) and ASC-CMed (p = 0.0121). The present study supports the anti-fibrotic effects of FGF-2 through the blockage of cardiac fibroblast differentiation into myofibroblasts. ASC-CMed, however, did not replicate the anti-fibrotic effects of FGF-2  in vitro .

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Fibroblast growth factor-2, but not the adipose tissue-derived stromal cells secretome, inhibits TGF-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts