MiR-155 deficiency protects renal tubular epithelial cells from telomeric and genomic DNA damage in cisplatin-induced acute kidney injury
Qing Yin, Yajie Zhao, Wei‐Jie Ni, Tao‐Tao Tang, Yao Wang, Jing-Yuan Cao, Di Yin, Yi Wen, Zuo‐Lin Li, Yilin Zhang, Wei Jiang, Yue Zhang, Xiaoyu Lu, Aiqing Zhang, Wei-Hua Gan, Lin‐Li Lv, Bi‐Cheng Liu, Bin Wang
Abstract
Rationale: Cisplatin nephrotoxicity is an important cause of acute kidney injury (AKI), limiting cisplatin application in cancer therapy. Growing evidence has suggested that genome instability, telomeric dysfunction, and DNA damage were involved in the tubular epithelial cells (TECs) damage in cisplatin-induced AKI (cAKI). However, the exact mechanism is largely unknown. Methods: We subjected miR-155 -/-mice and wild-type controls, as well as HK-2 cells, to cAKI models. We assessed kidney function and injury with standard techniques. The cell apoptosis and DNA damage of TECs were evaluated both in vivo and in vitro. Telomeres were measured by the fluorescence in situ hybridization.