转化生长因子β2对人晶状体上皮细胞间质转分化的影响

Effects of TGF-β2 on epithelial mesenchymal transition in human lens epithelial cells

目的:探讨转化生长因子β2(TGF-β2)对培养的人晶状体上皮细胞(HLECs)增殖及诱导HLECs间质转分化的影响。方法:体外培养HLECs,培养基加入不同质量浓度TGF-β2进行干预,采用MTT法测定TGF-β2对细胞增殖的影响;细胞免疫化学染色方法检测100ng/LTGF-β2作用后E-钙黏素(E-cadherin)、α平滑肌肌动蛋白(α-SMA)和F-肌动蛋白(F-actin)的表达;RT-PCR方法检测E-cadherin、α-SMAmRNA的表达。结果:经TGF-β2处理后的HLECs增殖受到抑制;TGF-β2减弱HLECsE-cadherin的表达,相对表达量为(10.674±3.233),较对照组的(23.352±4.192)减弱(t=4.232,P=0.013)。TGF-β2增加HLECsα-SMA和F-actin的表达,相对表达量分别为(17.613±4.272)、(15.857±4.121),较对照组的0、(4.272±1.538)增强(Z=12.537,P<0.001;t=7.186,P=0.004)。RT-PCR结果显示,TGF-β2组HLECsE-cadherinmRNA的相对表达量为(0.321±0.081),较对照组的(0.983±0.248)减弱(t=3.491,P=0.008);TGF-β2组细胞α-SMAmRNA相对表达量为(0.632±0.158),较对照组的(0.097±0.028)增强(t=5.365,P=0.005)。结论:TGF-β2可以抑制HLECs的增殖,诱导HLECs间质转分化,可能参与后囊膜混浊的形成。

Aim：To investigate the effects of transforming growth factor-β2（TGF-β2） on proliferation and epithelial mesenchymal transition（EMT） in human lens epithelial cells（HLECs）.Methods：HLECs were cultured and passaged.The HLECs were treated with different concentrations of TGF-β2 for indicated times.The cell survival rate was assayed by MTT.The expressions of α-SMA,E-cadherin and F-actin in the cells treated by 100 ng/L TGF-β2 were analyzed with immunohistochemistry.The expressions of α-SMA and E-cadherin mRNA were detected by RT-PCR.Results：The expressions of E-cadherin after treatment of TGF-β2 was （10.674±3.233）,which in control group was （23.352±4.192）（t=4.232,P=0.013）.The expressions of α-SMA and F-actin after treatment of TGF-β2 were （17.613±4.272）and （15.857±4.121）,respectively,which in control group were 0 and （4.272±1.538）（Z=12.537,P0.001;t=7.186,P=0.004）.RT-PCR showed that the expression of E-cadherin mRNA in TGF-β2 group was （0.321±0.081）,which in control group was （0.983±0.248）（t=3.491,P=0.008）.The expression of α-SMA mRNA in TGF-β2 group was （0.632±0.158）,which in control group was （0.097±0.028）（t=5.365,P=0.005）.Conclusion： TGF-β2 could suppress the proliferation and induce EMT of HLECs.EMT of HLECs may be involved in the pathogenesis of posterior capsular opacification.