KLF4 Activates Autophagy Via mTOR/P70S6K Pathway to Attenuate High Glucose-induced Podocyte Injury
Objective:To analyze the effect of Krüppel like factor 4(KLF4)on high glucose-induced podocyte injury and its related molecular mechanism.Methods:MPC5 cells were cultured in vitro and divided into control group(Control group),high glucose group(HG group),high glucose + empty plasmid control group(HG + NC group)and high glucose + KLF4 overexpres-sion group(HG + KLF4 group).The expression of KLF4 mRNA was detected by qRT-PCR,the proliferation activity was detected by CCK-8,the apoptosis was detected by Flow cytometry,and the expression level of related protein was detected by Western blot.Results:Compared with Control group,the expression of KLF4 mRNA and protein of MPC5 cells in HG group decreased,the prolifer-ation activity of MPC5 cells decreased,the apoptosis rate increased,the expression of synaptopdin,podocin,nephrin,microtubule associated protein light chain 3-Ⅱ(LC3-Ⅱ),Beclin1 protein in MPC5 cells decreased,and the expression of P62 protein,the ratio of phosphorylated mammalian target of rapamycin(p-mTOR)/mTOR and phosphorylated 70-kDa ribosomal protein S6 kinase(p-P70S6K)/P70S6K increased;The difference was statistically significant(P<0.05).Compared with HG Group,the expression of KLF4 mRNA and protein of MPC5 cells in HG + KLF4 group increased,the proliferation activity in MPC5 cell increased,the ap-optosis rate decreased,the expression of synaptopdin,podocin,nephrin,LC3-Ⅱand Beclin1 protein increased,and the expression of P62 protein,the ratio of p-mTOR/mTOR and p-P70S6K/P70S6K decreased;The difference was statistically significant(P<0.05).Conclusion:KLF4 attenuates high glucose-induced podocyte injury by activating podocyte autophagy,and its mechanism may be related to the regulation of mTOR/P70S6K signaling pathway.
NETL
NSTL
万方数据
维普
