Effect of advanced glycation end product receptor signal transduction on MCP-1 expression of podocyte induced by carboxymethyllysine
- VernacularTitle:晚期糖基化产物受体信号传导在羧甲赖氨酸诱导足细胞表达单核细胞趋化因子中的作用
- Author:
Leyi GU
;
Jiaqi QIAN
;
Zhaohui NI
;
Tomino YASUHIKO
- Publication Type:Journal Article
- Keywords:
Monocyte chemoattractant protein 1;
Glycosylation end products, advanced;
Reactive oxygen species;
Mitogen-activated protein kinases;
Podocyte
- From:
Chinese Journal of Nephrology
2005;0(11):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the signalling events follow the activation of RAGE in podocytes. Methods AGE and CML generated dichloroflurescin-sensitive intracellular ROS were measured by confocal microscopy. The activation of MAP kinases family were studied using Western blotting. MCP-1 mRNA expression was detected by semi-quantitative RT-PCR. Results Basal ROS was located in nucleus of starvation podocytes. AGE and CML rapidly generated intracellular ROS in podocytes. NAC pre-treated podocytes suppressed basal and inducible ROS generation and antibody for RAGE suppressed the inducible ROS. Blockage of ROS induced by NAC suppressed the expression of CML and H_2O_2-induced MCP-1. Phosphorylated extracellular signal-regulated kinase (ERK) was found in CML incubated podocytes at 10 min and was prevented by NAC or AFC. PD98058 Pre-treated podocytes partially inhibited the expression of CML-induced MCP-1 mRNA. No evidence were showed that p38 MAPK, SAPK/JNK, PI3K and PKC were involved in the signal transduction. Conclusion Activation of RAGE induces MCP-1 expression in podocytes via ROS-ERK signalling pathway.
