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The Study on the Action of p38-HSP27 Signaling Pathway Mediating the Actin Cytoskeleton Remodeling in Renal Tubular Epithelial Cells during ATP Depletion

Author: ZhangLiJia
Tutor: GuLuo
School: Nanjing Medical University
Course: Physiology
Keywords: ATP depletion Tubular epithelial cells Actin cytoskeleton p38 kinase Heat shock protein 27 (HSP27)
CLC: R692.6
Type: Master's thesis
Year: 2008
Downloads: 103
Quote: 0
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Previous studies confirmed ischemic renal injury, tubular epithelial cell actin cytoskeleton remodeling is impaired renal function worsening ischemic renal injury, specific mechanisms of actin cytoskeleton remodeling unclear. Renal ischemic state analog of this study, in vitro ATP depletion model based on study ATP depletion renal tubular epithelial cell actin cytoskeleton reconstruction of the situation and the actin cytoskeleton remodeling the possible mechanisms to a period of The pathogenesis of ischemic renal injury provides a theoretical basis. According to the results of previous studies, we speculate that the p38-HSP27 signaling pathway may be involved in ATP depletion of renal tubular epithelial cell actin cytoskeleton remodeling process. In this study the rat renal proximal tubular epithelial cell line (NRK52E cells), after fluorescent staining ATP missing actin cytoskeleton reconstruction; cells by immunoblotting p38 kinase expression and activity changes , simultaneous analysis of HSP27 expression, the change of the level of phosphorylation of its intracellular localization. F-actin protein staining results showed that ATP deletion NRK52E cell actin cytoskeleton significantly reconstructed F-actin protein content was significantly higher, and the processing time related to ATP depletion. This result indicates that the ATP depletion actin cytoskeleton occurs polymerized reconstructed changes. Western blot results showed that the ATP deletion of p38 kinase activated quickly, HSP27 phosphorylation was significantly strengthened, and HSP27 redistribution phenomenon from the skeleton components to the cytoplasmic constituents. After the use of the p38 kinase inhibitor SB203580 pretreatment of the cells of p38 kinase activity was able to significantly inhibit the phosphorylation of HSP27 of significant inhibition the heavy of HSP27 distribution phenomenon can be reversed; while ATP depletion due to the actin cytoskeleton constitutive phenomenon can be partially reversed by ATP missing due to F-actin content increased significantly inhibited. The results of this study show that the p38 kinase through the regulation of HSP27 phosphorylation state affects its weight distribution, and then participate in renal tubular epithelial cells in the reconstruction of the actin cytoskeleton partially mediated ATP depletion. Through the above research, we draw the following conclusions: 1.ATP missing tubular epithelial cell actin cytoskeleton polymerization occurs reconfigurable change. 2.p38-HSP27 signaling pathways involved in part mediated ATP depletion of renal tubular epithelial cell actin cytoskeleton reconstruction effect.

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CLC: > Medicine, health > Surgery > Urology ( urinary and reproductive system diseases) > Kidney disease > Renal tubular,glomerular disease
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