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MiR-106b-5p Inhibits Tumor Necrosis Factor-α-induced Apoptosis by Targeting phosphatase and tensin homolog deleted on chromosome 10 in Vascular Endothelial Cells

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Chinese Medical Journal 2016年第12期129卷 1406-1412页

作者： Jing Zhang Su-Fang Li Hong Chen Jun-Xian Song Department of Cardiology Peking University People's Hospital Beijing 100044 China Beijing Key Laboratory of Early Prediction and Intervention of Acute Myocardial Infarction Peking University People's Hospital Beijing 100044 China Center for Cardiovascular Translational Research Peking University People's Hospital Beijing 100044 China

Background： Apoptosis of endothelial cells （ECs） plays a key role in the development of atherosclerosis and there are also evidence indicated that phosphatase and tensin homolog deleted on chromosome 10 （PTEN） is a viable target in therapeutic approaches to prevent vascular ECs apoptosis. Aberrant miR-106b-5p expression has been reported in the plasma of patients with unstable atherosclerotic plaques. However, the role and underlying mechanism of miR-106-5p in the genesis of atherosclerosis have not been addressed. In this study, we explored the anti-apoptotic role of miR-106-5p by regulating PTEN expression in vascular ECs. Methods： Real-time reverse transcription polymerase chain reaction （RT-PCR） was performed to detect the expression levels of miR-106b-5p in human atherosclerotic plaques and normal vascular tissues. Human umbilical vein endothelial cells （HUVEC） were transfected with miR-106b-5p mimic or negative control mimic, and apoptosis was induced by serum starvation and tumor necrosis factor-α （TN F-α） treat. Western blotting and real-time RT-PCR experiments were used to detect PTEN expression levels and TN F-α-induced apoptosis was evaluated by the activation of caspase-3 and cell DNA fragmentation levels in HUVEC. Results： The expression ofmiR-106b-5p was significantly downregulated in plaques than in normal vascular tissues. TNF-α significantly downregulated miR-106b-5p expression levels and upregulated activation of caspase-3 and cell DNA fragmentation levels in HUVEC. Overexpression ofmiR-106b-5p with miR-106b-5p mimic inhibited PTEN expression and TNF-α-induced apoptosis in HUVEC. Luciferase reporter assays confirmed that miR-106b-5p binds to PTEN mRNA 3＇ untranslated region site, Conclusion： MiR-106b-5p could inhibit the expression of PTEN in vascular ECs, which could block TNF-α-induced activation of caspase-3, thus prevent ECs apoptosis in atherosclerosis diseases.

关键词： Apoptosis Atherosclerosis MicroRNAs phosphatase and tensin homolog deleted on chromosome 10

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Upregulated DJ-1 Promotes Renal Tubular EMT by Suppressing Cytoplasmic PTEN Expression and Akt Activation

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2011年第4期31卷 469-475页

作者：姚颖位红兰刘丽丽刘琳白寿军李彩霞罗云曾锐韩敏葛树旺徐钢 Department of Nephrology Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology

Recently,phosphatase and tensin homolog deleted on chromosome 10（PTEN） is suggested as a new agent in the fighting against fibrogenesis.In tumor,DJ-1 is identified as a negative regulator of PTEN.But the expression of DJ-1 and the regulation of PTEN in fibrosis are unclear.Renal fibrosis was induced in 5/6 subtotal nephrectomy rat model.Human proximal tubular epithelial cells（HKC） were treated with transforming growth factor-beta 1（TGF-β1）,or transfected with DJ-1 or PTEN.Confocal microscope was used to investigate the localization of DJ-1 and PTEN.The selective phosphoinositide-3 kinase（PI3K） inhibitor,LY294002,was administered to inhibit PI3K pathway.The DJ-1 and PTEN expression,markers of epithelial-mesenchymal transition（EMT） and Akt phosphorylation were measured by RT-PCR,Western blotting or immunocytochemistry.In vitro,after HKC cells were stimulated with 10 ng/mL TGF-β1 for 72 h,the expression of DJ-1 was increased,and that of PTEN was decreased.In vivo,the same results were identified in 5/6-nephrectomized rats.In normal HKC cells,most of DJ-1 protein localized in cytoplasm,and little in nucleus.TGF-β1 upregulated DJ-1 expression in both cytoplasma and nuclei.In contrary,TGF-β1 emptied cytoplasmic PTEN protein into nucleus.Overexpression of DJ-1 decreased the expression of PTEN,promoted the activation of Akt and the expression of vimentin,and also led to the loss of cytoplasmic PTEN.Contrarily,overexpression of PTEN protected HKC cells from TGF-β1-induced EMT.In conclusion,DJ-1 is upregulated in renal fibrosis and DJ-1 mediates EMT by suppressing cytoplasmic PTEN expression and Akt activation.

关键词： transforming growth factor-beta 1 DJ-1 phosphatase and tensin homolog deleted on chromosome 10 Akt epithelial-mesenchymal transition

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