LncRNA SNHG16 Aggravates High Glucose-Induced Podocytes Injury in Diabetic Nephropathy Through Targeting miR-106a and Thereby Up-Regulating KLF9
Xin He,1 Xiuya Zeng2 1Clinical Laboratory Center, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, Mainland China; 2Department of Clinical Laboratory (Xiamen Key Laboratory of Genetic Testing), The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003,...
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| Formato: | article |
| Lenguaje: | EN |
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Dove Medical Press
2020
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| Acceso en línea: | https://doaj.org/article/04a6bc7cf088444794c51dd20a1abb64 |
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| Sumario: | Xin He,1 Xiuya Zeng2 1Clinical Laboratory Center, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, Mainland China; 2Department of Clinical Laboratory (Xiamen Key Laboratory of Genetic Testing), The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003, Mainland ChinaCorrespondence: Xiuya ZengDepartment of Clinical Laboratory, The First Affiliated Hospital of Xiamen University, Siming District, Xiamen City, Fujian Province 361003, Mainland ChinaEmail zengxiuya1200@163.comIntroduction: Diabetic nephropathy (DN) is one of the major complications of diabetes and podocyte injury plays an important role in the DN pathogenesis. MicroRNA (miR)-106a is predicated to be a target of long noncoding RNA (lncRNA) SNHG16 and has been identified as a therapeutic biomarker for diabetic kidney diseases. However, the role of SNHG16/miR-106a axis in DN has not been illustrated. This study aimed to investigate whether SNHG16 could regulate podocyte injury via miR-106a in DN and uncover the underlying mechanism.Methods: MPC5 podocytes were treated with control or high glucose (HG) medium, and then miR-106a level was measured. MPC5 cells that exposed to HG were overexpressed with miR-106a or not, following by overexpression with or without KLF9 or SNHG16. Then, cell viability, apoptosis, reactive oxygen species and the protein expression of synaptopodin and podocin were evaluated.Results: MiR-106a was down-regulated in the serum of DN patients and HG-induced MPC5 podocytes. Overexpression of miR-106a suppressed HG-induced decrease in cell viability, Bcl-2, synaptopodin and podocin expression, increase in ROS, apoptotic cells, Bax and cleaved-caspase 3 expression. MiR-106a could bind to both KLF9 and lncRNA SNHG16, which were up-regulated in the serum of DN patients and HG-induced MPC5 podocytes. The level of miR-106a was decreased by SNHG16 overexpression and miR-106a overexpression reduced KLF9 expression. Furthermore, overexpression of KLF9 or SNHG16 blunted the protective effects of miR-106a on HG-induced MPC5 injury.Discussion: LncRNA SNHG16 could promote HG-stimulated podocytes injury via targeting miR-106a to enhance KLF9 expression. The intervention of SNHG16/miR-106a/KLF9 may be a therapeutic treatment for DN.Keywords: diabetic nephropathy, high glucose, long noncoding RNA, miR-106a, podocyte |
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