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• W2854408917 abstract "BACKGROUND:Renal podocyte damage plays a crucial role in the development of diabetic nephropathy. Genistein is derived from a leguminous plant, and MyD88 and TRIF are adaptor molecules in the Toll-like receptor (TLR) signaling pathway, which may play a role in autophagy. In this study, we utilized an in vitro high glucose (HG)-treated podocyte model to investigate the effects and underlying mechanisms of Genistein and MyD88 or TRIF siRNA induced autophagy and renal protection. MATERIAL AND METHODS:An immortalized mouse podocyte cell line was treated with HG, Genistein, chloroquine, and/or transfected with specific Myd88 and TRIF siRNAs. The formation of autophagosomes and related autophagic vacuoles were monitored by transmission electron microscopy. The expression of autophagy-related factors and podocyte structure and functional markers, including LC3, p62, p-mTOR, synaptopodin, and nephrin, were measured by Western blot, and LC3 and p-mTOR expression were also assessed by immunofluorescence. RESULTS:We showed that HG transiently (after 6-h exposure) induced expression of the autophagy activation marker LC3-II in podocytes. Genistein treatment induced autophagy in both normal and HG-treated podocytes through inactivating mTOR signaling. Moreover, Genistein protected podocytes against chloroquine in HG-cultured conditions in vitro by maintaining the level of autophagy-related proteins. In addition, MyD88 siRNA downregulated expression of autophagy-related proteins, whereas Genistein treatment reversed these effects. CONCLUSIONS:This study demonstrated that Genistein-induced autophagy could be a potential treatment strategy for glomerular diseases." @default.
• W2854408917 created "2018-07-19" @default.
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• W2854408917 date "2018-07-12" @default.
• W2854408917 modified "2023-10-17" @default.
• W2854408917 title "Genistein and Myd88 Activate Autophagy in High Glucose-Induced Renal Podocytes In Vitro" @default.
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• W2854408917 doi "https://doi.org/10.12659/msm.910868" @default.
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• W2854408917 hasPublicationYear "2018" @default.
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