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

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)-tr...