MiR-142-3p ameliorates high glucose-induced renal tubular epithelial cell injury by targeting BOD1

• Published in: Clinical and experimental nephrology Vol. 25; no. 11; pp. 1182 - 1192
• Main Authors: Zhao, Ningmin, Luo, Qing, Lin, Ruijuan, Li, Qiaoyan, Ma, Peizhi
• Format: Journal Article
• Language: English
• Published: Singapore Springer Singapore 01.11.2021; Springer Nature B.V
• Subjects: Animals; Apoptosis; Apoptosis - drug effects; Apoptosis - genetics; Blood Urea Nitrogen; Cell Cycle Proteins - genetics; Cell Cycle Proteins - metabolism; Cell division; Cell injury; Cell Line; Cell Survival - drug effects; Cell viability; Creatinine - blood; Diabetes mellitus; Diabetes Mellitus, Experimental - chemically induced; Diabetic Nephropathies; Diabetic nephropathy; Down-Regulation - drug effects; Down-Regulation - genetics; Enzyme-linked immunosorbent assay; Epithelial cells; Epithelial Cells - metabolism; Epithelial Cells - pathology; Flow cytometry; Gene Expression; Glucose - administration & dosage; Glucose - pharmacology; Humans; Kidney Tubules; Kidneys; Male; Medicine; Medicine & Public Health; MicroRNAs - genetics; MicroRNAs - metabolism; miRNA; Nephrology; Nephropathy; Original Article; Oxidative stress; Oxidative Stress - drug effects; Oxidative Stress - genetics; Rats; RNA, Messenger - metabolism; Streptozocin; Urology; Diabetic nephropathy; miR-142-3p; Renal tubular epithelial cell injury; BOD1
• ISSN: 1342-1751; 1437-7799; 1437-7799
• DOI: 10.1007/s10157-021-02102-y

Background Tubular injury plays a crucial role in the pathogenesis of diabetic nephropathy (DN). It is well known that many microRNAs (miRNAs) exert crucial effects on tubular injury. This study intends to explore the effect of miR-142-3p on the apoptosis and oxidative stress of high glucose (HG)-treated renal tubular epithelial cells (HK-2) and its underlying mechanism. Materials and methods HK-2 cells were exposed to HG to mimic cell injury. MTT assays and flow cytometry analyses were conducted to measure cell viability and cell apoptosis, respectively. RT-qPCR and western blot analyses were carried out to detect RNA and protein levels, respectively. The levels of oxidative stress markers were evaluated by ELISA. The binding between miR-142-3p and biorientation of chromosomes in cell division 1 (BOD1) was validated by a luciferase reporter assay. Result MiR-142-3p is low-expressed in HG-stimulated HK-2 cells. Functionally, miR-142-3p overexpression attenuates the apoptosis and oxidative stress of HG-stimulated HK-2 cells. Mechanistically, BOD1 was confirmed to be targeted by miR-142-3p in HK-2 cells. Moreover, BOD1 overexpression reversed the suppressive effect of miR-142-3p overexpression on the apoptosis and oxidative stress of HK-2 cells treated with HG. Conclusion MiR-142-3p ameliorates HG-induced renal tubular epithelial cell injury by targeting BOD1. The finding might provide novel insight into the role of miR-142-3p/BOD1 axis in DN treatment.