Role of ROCK1 in the podocyte injury induced by oxidized low-density lipoprotein
10.3760/cma.j.issn.1001-7097.2017.01.006
- VernacularTitle: RhoA激酶1在氧化低密度脂蛋白诱导足细胞损伤中的作用
- Author:
Menglei JU
1
;
Huizhen WANG
;
Yangyang ZUO
;
Jianteng XIE
;
Feng WEN
;
Sheng LI
;
Lei FU
;
Jing LI
;
Tiantian LIANG
;
Yanhui WANG
;
Wei SHI
;
Wenjian WANG
Author Information
1. Southern Medical University, Guangzhou 510515, China
- Publication Type:Journal Article
- Keywords:
Podocytes;
Lipoproteins, LDL;
Autophagy;
rho-associated kinases;
LC3-Ⅱ
- From:
Chinese Journal of Nephrology
2017;33(1):37-42
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the role of ROCK1 in oxidized low-density lipoprotein (ox-LDL) induced podocyte injury and its possible mechanism.
Methods:The conditionally immortalized mouse podocyte cells were cultured in vitro and exposed to 20 μg/ml ox-LDL for 24 h. Western blotting was used to analyze the expression level of p-MYPT, nephrin, LC3-Ⅱ, p62, p-ULK1 in groups of control, ox-LDL, ROCK1 siRNA with ox-LDL, wtROCK1 with ox-LDL. Podocytes were incubated with DiI labeled ox-LDL for 4 h and fluorescence microscope was used to analyze lipid distribution.
Results:Compared with control group, ox-LDL increased cell cholesterol accumulation, activated ROCK along with decreased nephrin, LC3-Ⅱ(P<0.05), and increased p62, and p-ULK1 expression (P<0.05). Over-expression of ROCK1 significantly decreased the expression of nephrin and LC3-Ⅱ, but up-regulated the levels of p62, p-ULK1 and cell cholesterol accumulation in ox-LDL stimulated podocytes (P<0.05). In contrast, Inhibition of ROCK1 protected podocyte by improved lipophagy.
Conclusion:ROCK1 mediated disfunction of lipophagy contributes to the ox-LDL induced podocyte injury.
