LncRNA SOX2OT alleviates the high glucose-induced podocytes injury through autophagy induction by the miR-9/SIRT1 axis
| Autor: | Yan Zhang, Baochao Chang, Xue-ping Wu, Jiqiang Zhang |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Clinical Biochemistry Autophagy-Related Proteins Apoptosis Pathology and Forensic Medicine Flow cytometry Diabetic nephropathy 03 medical and health sciences 0302 clinical medicine Western blot Sirtuin 1 medicine Autophagy Humans MTT assay Luciferase Molecular Biology Cells Cultured Cell Proliferation Gene knockdown medicine.diagnostic_test Chemistry Podocytes medicine.disease Cell biology MicroRNAs 030104 developmental biology Glucose Gene Expression Regulation 030220 oncology & carcinogenesis RNA Interference RNA Long Noncoding Signal Transduction |
| Zdroj: | Experimental and molecular pathology. 110 |
| ISSN: | 1096-0945 |
| Popis: | Objectives Podocytes injury is a major contributor to the progression of diabetic nephropathy (DN). This study aims to investigate the role of long non-coding RNA SOX2OT in the high glucose (HG)-induced injury of human podocytes cells (HPCs) and the underlying mechanism. Methods HPCs proliferation and apoptosis were examined using MTT assay and flow cytometry assay, respectively. The protein levels of SIRT1 and autophagy-associated proteins (Beclin-1, LC3-II, Atg7, and p62) were determined using western blot. The interactions among SOX2OT, miR-9, and SIRT1 were investigated using luciferase activity assay. Results SOX2OT overexpression significantly alleviated the HG-induced HPCs injury and induced autophagy, which was abrogated by the autophagy inhibitor 3-MA and SIRT1 knockdown. Mechanistically, SOX2OT acted as a ceRNA by sponging miR-9 to facilitate SIRT1, and thus induce autophagy. Conclusion SOX2OT overexpression alleviates the HG-induced podocytes injury through autophagy induction by the miR-9/SIRT1 axis. |
| Databáze: | OpenAIRE |
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