Objective:To investigate the effect of activin A(ACT A)on microvascular endothelial cell transdifferentiation(EndMT)and the intervention of follistatin(FS).Methods:(1)Human umbilical vein endothelial cells(HUVEC)were cultured in vitro.The proliferation rate of HUVEC stimulated by rh-ACT A and rh-FS was measured by MTT assay.(2)Cells were divided into 5 groups: control group(group C),TGF-β group(group T),ACT A group(group A),TGF-β+FS group(group T+F),ACT A+FS group(group A+F).The effects of ACT A and TGF-β on the expression of α-smooth muscle actin(α-SMA),VE-cadherin(VE-cad)and fibronectin(FN)in HUVEC cells were observed by cytochemical staining and Western blotting.Results:(1)Compared with 0ng/L ACT A group,the proliferation activity of 10ng/L ACT A group,30ng/L ACT A group,60ng/ml ACT A group and 100ng/m ACT A group increased(F=22.768,P<0.001).The proliferation rate of 30ng/L ACT A group was the highest,and FS alone had no significant effect on cell proliferation(F=0.437,P=0.781).However,FS could antagonize the effect of ACT A on the growth of endothelial cells in a dose-dependent manner(F=15.270,P<0.001).(2)Cytochemical staining and Western blotting showed that the expression of α-SMA and FN increased,while the expression of VE-Cad decreased(P<0.05)after ACT A stimulated endothelial cells.Compared with TGF-β group,no statistically significant difference in the expression of α-SMA,FN and VE-Cad(P>0.05).But there was no significant effect on TGF-β.Compared with ACT A group,the expression of α-SMA and FN decreased and the expression of VE-Cad increased in ACT A+FS group(P<0.05).There was no significant difference in the expression of α-SMA,FN and VE-Cad between TGF-β+FS group and TGF-β group(P>0.05).Conclusion:ACT A can induce endothelial cell transdifferentiation and FN synthesis,and FS can block the above effects of ACT A and produce endothelial protection. |