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


CONCLUSIONS
KIM-1 may mediate high glucose-induced autophagy and apoptosis in renal tubular epithelial cells.
Rong
R
Gou
Juntong
J
Chen
Shifeng
S
Sheng
Ruiqiang
R
Wang
Yudong
Y
Fang
Zijun
Z
Yang
Liuwei
L
Wang
Lin
L
Tang
D017209:Apoptosis; D001343:Autophagy; D002460:Cell Line; D004847:Epithelial Cells / Q000166:cytology* / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D000072596:Hepatitis A Virus Cellular Receptor 1 / Q000378:metabolism*; D006801:Humans; D007684:Kidney Tubules / Q000166:cytology* / Q000378:metabolism
C491143:HAVCR1 protein, human; D000072596:Hepatitis A Virus Cellular Receptor 1; D005947:Glucose