KIM-1 Mediates High Glucose-Induced Autophagy and Apoptosis in Renal Tubular Epithelial Cells

• Main Authors: Rong Gou, Juntong Chen, Shifeng Sheng, Ruiqiang Wang, Yudong Fang, Zijun Yang, Liuwei Wang, Lin Tang
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2016-06-01
• Series: Cellular Physiology and Biochemistry
• Subjects: LC3II; Diabetic nephropathy; Autophagosome; Renal fibrosis
• Online Access: http://www.karger.com/Article/FullText/445598
• ISSN: 1015-8987; 1421-9778

Background/Aim: To investigate the role of kidney injury molecular 1 (KIM-1) in high glucose-induced autophagy and apoptosis in renal tubular epithelial cells. Methods: Human renal tubular epithelial cells (HK2) were treated with normal glucose (NG, D -glucose 5.6 mmol/L), high glucose (HG, 30 mmol/L), high osmotic (HO, D-glucose 5.6 mmol/L + D-mannitol 24.4 mmol/L), HG + KIM-1 siRNA, HG + siRNA control. The expressions of KIM-1 and microtubule-associated protein 1 light chain 3II (LC3II) were measured by western blot as well as real time PCR; the number of autophagosome was detected by electron microscopy; and the level of apoptosis was analyzed by flow cytometry. Results: In the HG group, the expressions of KIM-1 and LC3II were increased markedly, which was accompanied by more autophagosome and higher level of apoptosis compared with NG group. Silencing of KIM-1 by siRNA inhibited the increases in the levels of LC3II, autophagosome and apoptosis. Conclusion: KIM-1 may mediate high glucose-induced autophagy and apoptosis in renal tubular epithelial cells.