Effect Of Ang-(1-7) On The Proliferation And Synthesis Of Collagen In Cultured Rat Cardiac Fibroblast Induced By TGF-β₁

objective: To investigate the role of Ang-(1-7) in the proliferation and synthesis of collagen in cultured rat cardiac fibroblast induced by TGF-β1, and to evaluate whether its possible intracellular signaling pathway is mediated by cAMP/PKA. Methods:Neonatal rat cardiac myofibroblasts were isolated and culture in vitro. The influence of Ang-(1-7) on cardiac myofibroblasts proliferation was determined by WST-1 assay.The protein content of PCⅢin the cultured medium of treated groups and control groups was determined by radioimmunoassay. The experiment was divided into four parts. The first part, there were five groups: blank control group, different concentration(10-9-10-6mol/L) Ang-(1-7), in the part to investigate the influence of Ang-(1-7) on the cultured rat cardiac myofibroblasts in basic state. The second part, six groups: blank control group, different concentration(10-9-10-6mol/L) Ang-(1-7)+ TGF-β1 (5μg/L) groups and TGF-β1(5μg/L), to investigate the effect of different concentration Ang-(1-7) on cardiac myofibroblasts induced by TGF-β1. The third part, four groups: blank control group, Ang-(1-7) group, H-89 group as well as H-89+ Ang-(1-7) group. The fourth part, five groups: blank control group, TGF-β1+ H-89 group, TGF-β1+ Ang-(1-7) group, TGF-β1+ Ang-(1-7) + H-89 group. Conclusion: 1) Ang-(1-7) can inhibit the proliferation and synthesis of collagen in cardiac myofibroblasts in the basic state. 2) Ang-(1-7) can inhibit the proliferation and synthesis of collagen in cardiac myofibroblasts induced by TGF-β1. 3) The PKA pathway is likely to involved with the proliferation and synthesis of collagen in cardiac myofibroblasts induced by TGF-β1.