Gou Rong, Chen Juntong, Sheng Shifeng, Wang Ruiqiang, Fang Yudong, Yang Zijun, Wang Liuwei, Tang Lin
Cell Physiol Biochem. 2016;38(6):2479-88. doi: 10.1159/000445598. Epub 2016 Jun 17.
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.
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.
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.
KIM-1 may mediate high glucose-induced autophagy and apoptosis in renal tubular epithelial cells.
背景/目的：探讨肾损伤分子1（KIM-1）在高糖诱导的肾小管上皮细胞自噬和凋亡中的作用。
将人肾小管上皮细胞（HK2）分别用正常葡萄糖（NG，D-葡萄糖5.6 mmol/L）、高糖（HG，30 mmol/L）、高渗（HO，D-葡萄糖5.6 mmol/L + D-甘露醇24.4 mmol/L）、HG + KIM-1小干扰RNA（siRNA）、HG + 对照siRNA处理。采用蛋白质免疫印迹法及实时定量聚合酶链反应检测KIM-1和微管相关蛋白1轻链3II（LC3II）的表达；通过电子显微镜检测自噬体数量；采用流式细胞术分析凋亡水平。
与NG组相比，HG组KIM-1和LC3II的表达显著增加，同时伴有更多的自噬体和更高水平的凋亡。siRNA沉默KIM-1可抑制LC3II水平、自噬体数量及凋亡的增加。
KIM-1可能介导高糖诱导的肾小管上皮细胞自噬和凋亡。
