Abstract:
:Cardiac fibroblast (CF) proliferation and transformation into myofibroblasts play important roles in cardiac fibrosis during pathological myocardial remodeling. In this study, we demonstrate that hepatocyte growth factor (HGF), an antifibrotic factor in the process of pulmonary, renal and liver fibrosis, is a negative regulator of cardiac fibroblast transformation in response to transforming growth factor‑β1 (TGF‑β1). HGF expression levels were significantly reduced in the CFs following treatment with 5 ng/ml TGF‑β1 for 48 h. The overexpression of HGF suppressed the proliferation, transformation and the secretory function of the CFs following treatment with TGF‑β1, as indicated by the attenuated expression levels of α-smooth muscle actin (α‑SMA) and collagen I and III, whereas the knockdown of HGF had the opposite effect. Mechanistically, we identified that the phosphorylation of c‑Met, Akt and total protein of TGIF was significantly inhibited by the knockdown of HGF, but was significantly enhanced by HGF overexpression. Collectively, these results indicate that HGF activates the c‑Met‑Akt‑TGIF signaling pathway, inhibiting CF proliferation and transformation in response to TGF‑β1 stimulation.
journal_name
Int J Mol Medjournal_title
International journal of molecular medicineauthors
Yi X,Li X,Zhou Y,Ren S,Wan W,Feng G,Jiang Xdoi
10.3892/ijmm.2014.1782subject
Has Abstractpub_date
2014-08-01 00:00:00pages
381-90issue
2eissn
1107-3756issn
1791-244Xjournal_volume
34pub_type
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