Smad3信号通路及其靶基因CTGF在豚鼠巩膜成纤维细胞的表达

Expression of Smad3 signal way and CTGF in scleral fibroblasts of guinea pigs

目的:探讨结缔组织生长因子(CTGF)参与形觉剥夺性近视的可能机制.方法:采用对照实验性研究.用MTT比色法检测不同浓度的外源性转化生长因子(TGF-β1)干预前后豚鼠巩膜成纤维细胞(GSF)增生的质量浓度效应和时间效应,RT-PCR检测GSF中CTGF以及smad3mRNA的表达,Western Blot检测CTGF以及smad3蛋白的表达.结果:在0.1～50μg/L浓度范围内,TGF-β1可促进巩膜成纤维细胞增生(P<0.05);干预前后均可见到CTGF及smad3的表达;干预后CTGF及smad3 mRNA和蛋白表达量明显高于干预前.结论:TGF-β1可以上调CTGF及smad3的表达.

AIM： To investigate the possible mechanism of Smad3 signal way and CTGF in the development of form deprivation myopia （FDM） by detecting the expression of CTGF and Smad3 in scleral fibroblast of guinea pigs （GSF） in vitro. METHODS： RT-PCR was used to detect the mRNA of CTGF and Smad3 and Western Blot was used to determine the protein levels of CTGF and Smad3 in scleral fibroblasts. RESULTS： Western Blot and RT-PCR revealed that CTGF and Smad3 protein and mRNA were up-unregulated in the cells induced by TGF-~I. The results of MTr showed that TGF-β significantly induced fibroblasts proliferation. CONCLUSION： TGF-β1 up-regulates the expression of CTGF and Smad3.