【摘要】 目的探讨miR-222是否通过靶向调控TIMP3表达参与糖尿病肾病的发生过程,从而进一步揭示糖尿病肾病的发病机制。方法运用qRT-PCR检测经25 mmol/L葡萄糖处理的小鼠系膜细胞(HG组)和对照小鼠系膜细胞(5 mmol/L葡萄糖,NG组)中miR-222和TIMP3的表达;将miR-222 mimics转染小鼠系膜细胞,以TIMP3 siRNA为阳性对照,采用Western blot检测其对TIMP3蛋白表达水平的影响。结果 qRT-PCR检测结果显示,miR-222在经高糖处理的小鼠系膜细胞中的表达相对比正常浓度糖处理的小鼠系膜细胞中明显上调,而TIMP3在经高糖处理的小鼠系膜细胞中mRNA的表达相对比正常浓度糖处理的小鼠系膜细胞中明显下调;Western blot结果显示,过表达miR-222或干扰TIMP3可抑制TIMP3蛋白的表达(P<0.05)。结论 miR-222可能通过调控TIMP3的表达参与糖尿病肾病的发生发展。更多还原

【Abstract】 Objective To explicit whether miR-222 involved in diabetic nephropathy progression by targeting TIMP3,thus to reveal molecular mechanism of diabetic nephropathy. Methods A qRT-PCR was conducted for detect the expression of miR-222 and TIMP3 mRNA in high glucose condition( 25 mmol /L glucose) and normal glucose condition( 5mmol /L glucose) in SV40 MES 13 mouse mesangial cells. SV40 MES 13 mouse mesangial cells were transfected with miR-222 mimics,and TIMP3 siRNA as for positivecontrol,Western blot was performed to detect the expressions of TIMP3 protein. Results qRT-PCR showed that miR-222 was up-regulated in high glucose condition,however,the mRNA of TIMP3 was down-regulated in high glucose condition. Western blot showed that the expressions of TIMP3 protein was inhibited by transfected with miR-222 or siR TIMP3 in SV40 MES 13 mouse mesangial cells. Conclusion miR-222 may involvedin diabetic nephropathy progression by regulating TIMP3.更多还原