Yan Zhang1, Baochao Chang2, Jiqiang Zhang2, Xueping Wu2. 1. Departments of Nephrology, The First Affiliated Hospital of Bengbu Medical College, No. 287 Changhuai Road, Bengbu, Anhui 233000, PR China. Electronic address: zhang_yan18@163.com. 2. Departments of Nephrology, The First Affiliated Hospital of Bengbu Medical College, No. 287 Changhuai Road, Bengbu, Anhui 233000, PR China.
Abstract
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.
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.