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首页> 美国卫生研究院文献>Scientific Reports >Fibroblast growth factor-2 but not the adipose tissue-derived stromal cells secretome inhibits TGF-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts
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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

机译：成纤维细胞生长因子2（而非脂肪组织来源的基质细胞分泌组）抑制TGF-β1诱导的人心脏成纤维细胞向肌成纤维细胞的分化

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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.
机译：转化生长因子-β1（TGF-β1）是成纤维细胞对成肌纤维细胞分化的有效诱导剂，在心脏重塑过程中有助于促纤维化微环境。成纤维细胞生长因子2（FGF-2）是脂肪组织来源的基质细胞（ASC）分泌的生长因子，可拮抗TGF-β1信号传导。我们假设FGF-2和ASC条件培养基（ASC-CMed）废除了TGF-β1诱导的心脏成纤维细胞向成肌纤维细胞的分化。我们的实验表明，TGF-β1治疗可诱导心脏成纤维细胞分化为成肌纤维细胞，这可通过富含αSMA的收缩应激纤维的形成来证明。 FGF-2阻止了分化，这由间充质标记的基因（TAGLN，p，<0.0001； ACTA2，p = 0.0056）和蛋白质（αSMA，p = 0.0338）的减少以及细胞外基质成分基因表达（COL1A1，p <0.0001； COL3A1，p = 0.0029）。 ASC-CMed不阻止成肌纤维细胞分化。 FGF-2处理可增加基质金属蛋白酶基因表达（MMP1，p 0.0001； MMP14，p = 0.0027），并降低组织蛋白酶金属蛋白酶基因TIMP2的表达（p = 0.0023）。 ASC-CMed不影响这些基因。 FGF-2（p = 0.0002）和ASC-CMed（p = 0.0121）均可恢复TGF-β1诱导的人心脏成纤维细胞的增殖。本研究通过阻止心脏成纤维细胞分化为成肌纤维细胞，支持FGF-2的抗纤维化作用。然而，ASC-CMed不能在体外复制FGF-2的抗纤维化作用。

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