TRB3在肾纤维化中的表达及其与上皮-间叶转化的关系

目的研究TRB3与肾纤维化的关系和作用机制。方法结扎♂性C57BL/6小鼠单侧输尿管,建立肾纤维化模型。利用H&E染色和Masson染色确立纤维化病变。在过表达TRB3条件下,利用免疫印迹检测E-cadherin和α-SMA表达改变。在干扰TRB3条件下,利用细胞划痕实验检测细胞迁移。结果肾纤维化模型组TRB3蛋白表达高于假手术组(P<0.01),且与纤维化严重程度正相关。在大鼠肾小管上皮细胞NRK中过表达TRB3,导致E-cadherin表达降低,而α-SMA表达增高。干扰TRB3降低TGF-β1诱导的HepG2细胞迁移。结论 TRB3在纤维化肾脏组织中表达增高。TRB3可能通过诱导上皮-间叶转化在纤维化的进展中发挥促进作用。

Expression of TRB3 in renal fibrosis andits relation with epithelial-mesenchymal transition

Aim To study the effect of TRB3 on renal fibrosis and its mechanism.Methods Male C57BL/6 mice were subjected to unilateral ureteral obstruction(UUO) procedure to establish renal fibrosis.The interstitial fibrotic lesions of obstructed kidneys were evaluated with histology.The expression of E-cadherin and α-SMA were analyzed with immunoblotting when overexpressing TRB3.The migratory ability of cells was detected by wound-healing assay when silencing TRB3.Results TRB3 was significantly increased in mice with renal fibrosis and the expression level was increased during the progression of fibrosis.Overexpression of TRB3 in NRK cells increased the expression of α-SMA but inhibited the expression of E-cadherin.Depletion of TRB3 inhibited the migration of HepG2 cells induced by TGF-β1.Conclusion TRB3 is upregulated in kidney of mice with renal fibrosis.TRB3 acts as an inducer of epithelial-mesenchymal transition which may participates in the renal fibrosis progression.