FAN Yan-hong, DONG Hui, PAN Qing, GUO Wen-yi, WANG Hai-chang. Role of transforming growth factor β1 in differentiation of cardiac fibroblasts induced by arginine vasopressin[J]. Chinese Heart Journal, 2012, 24(1): 7-11. DOI: 10.13191/j.chj.2012.01.13.fanyh.007
    Citation: FAN Yan-hong, DONG Hui, PAN Qing, GUO Wen-yi, WANG Hai-chang. Role of transforming growth factor β1 in differentiation of cardiac fibroblasts induced by arginine vasopressin[J]. Chinese Heart Journal, 2012, 24(1): 7-11. DOI: 10.13191/j.chj.2012.01.13.fanyh.007

    Role of transforming growth factor β1 in differentiation of cardiac fibroblasts induced by arginine vasopressin

    • AIM:To investigate the role of transforming growth factor β1(TGF-β1) in the differentiation of cardiac fibroblasts(CFs) into myofibroblasts(MFs) induced by arginine vasopressin(AVP).METHODS:CFs were isolated by trypsin digestion method and co-incubated for 48 h with different concentrations of AVP,different concentrations of TGF-β1,or 1×10-6 mmol/L AVP supplemented with different concentrations of TGF-β1 neutralizing antibody,respectively.3H proline incorporation was used to measure collagen synthesis,Western blot analysis was used to measure α-smooth muscle actin(α-SMA) expression,and ELISA was used to measure TGF-β1 secretion in CFs.RESULTS:AVP induced the increases of 3H proline incorporation and α-SMA expression dose dependently in CFs,and 1×10-6 mol/L AVP notably increased 3H proline incorporation and α-SMA expression compared with those in control group(P<0.05).AVP induced endogenous TGF-β1 secretion of CFs dose dependently,and the notably increased endogenous TGF-β1 induced by 1×10-6 mol/L AVP was well within the range for exogenous TGF-β1 to cause differentiation of CFs into MFs(>2 ng/ml).Although 1×10-6 mol/L AVP-induced increases of 3H proline incorporation and α-SMA expression could be notably inhibited by TGF-β1 neutralizing antibody(P<0.05),they were still higher than those in control group(P<0.05).CONCLUSION:AVP can induce differentiation of CFs into MFs partly through the increase of endogenous TGF-β1 synthesis.
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