KIM-1 Mediates High Glucose-Induced Autophagy and Apoptosis in Renal Tubular Epithelial Cells
KIM-1 Mediates High Glucose-Induced Autophagy and Apoptosis in Renal Tubular Epithelial Cells
复制标题
KIM-1 介导高糖诱导的肾小管上皮细胞自噬和凋亡
DOI：
10.1159/000445598
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发表时间：
2016-01-01
影响因子：
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通讯作者：
Tang, Lin
中科院分区：
文献类型：
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作者：
Gou, Rong;Chen, Juntong;Tang, Lin
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。研究方法：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 siRNA、HG + siRNA对照组处理人肾小管上皮细胞（HK 2）。Western blot和真实的时间PCR检测KIM-1和微管相关蛋白1轻链3 Ⅱ（LC 3 Ⅱ）的表达;电镜观察自噬体的数量;流式细胞仪检测细胞凋亡水平。结果如下：与NG组相比，HG组KIM-1、LC 3 Ⅱ表达明显增加，自噬体增多，细胞凋亡水平升高。通过siRNA沉默KIM-1抑制LC 3 II、自噬体和凋亡水平的增加。结论：KIM-1可能介导高糖诱导的肾小管上皮细胞自噬和凋亡。
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.