Kidney injury molecule-1 is involved in the apoptosis of renal tubular cell line HK-2 induced by iodine contrast

Abstract

Objective To explore the role and the possible mechanism of kidney injury molecule-1(KIM-1) in the contrast-induced apoptosis of renal tubular epithelial cell. Methods Renal tubular epithelial cells line HK-2 was treated with contrast iohexol (75 mg/mL) and the expression of KIM-1 was examined by Western blot. The siRNA sequences were designed to interfere with KIM-1 gene expression. HK-2 cells were divided into four groups: control group (A), contrast group (B), contrast/vehicle group (C) and contrast/KIM-1-siRNA group (D). Each group was treated with 75 mg/mL iohexol for 2 h except control group. Flow cytometry and Bax and Bcl-2 protein expression were used to evaluate cell apoptosis. MDA, ROS,SOD,MDA, and MCP-1 were also examined in each group to evaluate the possible mechanism of KIM-1 involving in renal tubular epithelial cell injury induced by contrast agent. Results The expression of KIM-1 in HK-2 cells increased under iohexol exposure and reached the peak at 2 h. Iohexol treatment induced the apoptosis of HK-2 cells significantly. Meanwhile, the up-regulation of ROS and MCP-1 as well as the down-regulation of SOD and MDA was found(P＜ 0.05). Knockdown of KIM-1 by siRNA relieved the iohexol-induced apoptosis of HK-2 cells and partly dampened the up-regulation of ROS and MCP-1 and the down-regulation of SOD and MDA. Conclusions Iohexol can stimulate the expression of KIM-1 in renal tubular epithelial cells. KIM-1 may function in contrast-induce apoptosis of renal tubular epithelial cells by promoting oxidative stress and inflammatory reaction.

Keywords

• contrast-induced nephropathy|kidney injury molecule-1|renal tubular epithelial cell|apoptosis|oxidative stress