AIM: To explore the role of placental growth factor (PLGF) in theprocess of angiotensin Ⅱ (Ang Ⅱ) induced cardiac fibroblasts (CFs)activation.METHODS: Primary culture and identification cardiacfibroblasts(CFs) of neonatal Sprague-Dawley rats were performed.Fluorescence immunocytochemistry was employed to observealpha-smooth muscle actin (alpha-SMA). Real-time PCR and Western blotwere used respectively to determine mRNA and protein levels. WST-1wasadopted to assess cell proliferation.RESULTS:(1) To compare with that of in control, the PLGFmRNA(P<0.05) in AngⅡ treatment CFs was significantly increased,whereas in CFs treatment with telmisartan and AngⅡ in combinationPLGF mRNA was decreased.(2) Incubation with PLGF, the cell proliferation was induced andα-SMA protein expression was upregulated in CFs(P<0.05). Treatmentwith PLGF for60minutes, the protein expression levels of p-ERK1/2inCFs were significantly upregulated(P<0.05). (3) To compare with that of AngⅡ treated sole, cell proliferation wasdepressed and α-SMA protein expression was attenuated in CFs whentreated with AngⅡ and anti-PLGF in combination(P<0.05), and the geneexpression levels of type Ⅰ and type Ⅲ collagen were alsodownregulated(P<0.05).CONCLUSION: These data suggested that PLGF might be involvedin the processes of Ang Ⅱ-induced cell proliferation and fibrosis. |