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• W2013762364 abstract "<i>Background:</i> The apoptosis of podocytes is a characteristic event in diabetic nephropathy. The aim of this study was to investigate whether microRNAs (miRNAs) affect podocyte apoptosis in diabetic circumstances. <i>Methods:</i> Diabetic nephropathy was induced in DBA/2 mice by intraperitoneal injections of streptozotocin, and the levels of proteinuria were measured with ELISA. Apoptosis-related miRNAs were screened in isolated glomeruli. A conditionally immortalized mouse podocyte cell line was cultured in 25 m<i>M</i><i>D</i>-glucose and either transfected with miRNA-195 (miR-195) mimics or inhibitors. The levels of BCL2 and caspase expression were determined using real-time RT-PCR and Western blot analysis, respectively. We also measured WT-1 and synaptopodin in podocytes. Apoptosis of podocytes was assessed with Hoechst 33258 nuclear staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and flow cytometry. <i>Results: </i>The expression of miR-195 was elevated in both diabetic mice with proteinuria and podocytes that were cultured in high glucose. Transfection with miR-195 reduced the protein levels of BCL2 and contributed to podocyte apoptosis via an increase in caspase-3. miR-195-treated podocytes underwent actin rearrangement and failed to synthesize sufficient levels of WT-1 and synaptopodin proteins, which suggests that the cells had suffered injuries similar to those observed in diabetic nephropathy in both humans and animal models. <i>Conclusions:</i> Taken together, our findings demonstrate that miR-195 promotes apoptosis of podocytes under high-glucose conditions via enhanced caspase cascades for BCL2 insufficiency. This work thus presents a meaningful approach for deciphering mechanisms, by which miRNAs participate in diabetic renal injury." @default.
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• W2013762364 date "2011-01-01" @default.
• W2013762364 modified "2023-10-17" @default.
• W2013762364 title "MicroRNA-195 Promotes Apoptosis in Mouse Podocytes via Enhanced Caspase Activity Driven by BCL2 Insufficiency" @default.
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• W2013762364 doi "https://doi.org/10.1159/000333809" @default.
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