Effect of epidermal growth factor on glomerular epithelial cells cytoskeleton
- VernacularTitle:表皮生长因子对肾小球上皮细胞骨架的影响
- Author:
Ying WU
;
Hong XU
- Publication Type:Journal Article
- Keywords:
Epidermal growth factor;
Cytoskeleton;
Adriamycin;
Glomerular epithelial cell
- From:
Chinese Journal of Nephrology
2005;0(07):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the changes of adriamycin-induced glomerular epithelial cells (GECs) permeability and cytoskeleton, and to explore the role and possible mechanism of epithelia growth factor (EGF) on adriamycin-induced glomerular epithelial barrier function. Methods Rat GECs on Milicell-PCF Inserts were exposed to adriamycin (0.5 ?mmol/L) 24 hours in the absence or presence of EGF. The paracelluar permeability to BSA and cell viability were evaluated. The expression of F-actin and alpha-actinin were analyzed by immunofluorescence and Leica laser scan confocal microscopy. Results After induced by adriamycin for 24 hours, paracelluar permeability to BSA and F-actin reorganization rate increased. Disassembling of cortical cytoskeleton architecture was observed. Stress fiber in cytoplasm disappeared. Alpha-actinin staining showed perinuclear enhancement, which is different from normal cytosolic pattern. EGF significantly reduced adriamycin induced effect. Higher level of BSA passed through GEC monolayer in a dose-dependent manner. EGF prevented adriamycin-induced cytoskeletal reorganization. Disassembled cortical cytoskeleton was recovered, and stress fiber appeared again. Alpha-actinin staining mainly exhibited cytosolic uniform distribution as control GEC. In addition, administration of either AG1478, a specific inhibitor of EGF-receptor tyrosine kinase, or U73122, a specific inhibitor of PLC? before EGF treatment attenuated the EGF-mediated effect, whereas neither AG1478 nor U73122 exerted influence in the absence of EGF. Conclusions Adriamycin increases GEC paracellular permeability to BSA as a result of adriamycin-induced cytoskeleton disassembling and disruption. EGF may prevent adriamycininduced cytoskeleton reorganization and maintain glomerular epithelial barrier function through EGF mediated EGF-EGFR-PLC? signal pathway.
