Involvement of the PI3K/Akt Signaling Pathway in Platelet-Derived Growth Factor-Induced Migration of Human Lens Epithelial Cells

被引：37
作者：
Xiong, Wei [1 ]
Cheng, Bai-Hua [1 ]
Jia, Song-Bai [1 ]
Tang, Luo-Sheng [1 ]
机构：
[1] Cent S Univ, Dept Ophthalmol, Xiang Ya Hosp 2, Changsha, Hunan, Peoples R China
来源：
CURRENT EYE RESEARCH | 2010年 / 35卷 / 05期
关键词：
Migration of lens epithelial cell; PI3K/Akt pathway; PDGF; Posterior capsular opacification; POSTERIOR CAPSULAR OPACIFICATION; BETA-CATENIN; PHOSPHATIDYLINOSITOL; 3-KINASE; PROLIFERATION; PDGF; CANCER; PHOSPHORYLATION; DIFFERENTIATION; KINASE; TRANSDUCTION;
D O I：
10.3109/02713680903584686
中图分类号：
R77 [眼科学];
学科分类号：
100212 ;
摘要：
Purpose: Posterior capsular opacification (PCO) is caused partially by the migration of lens epithelial cells. To date, the mechanism of the migration is largely unknown. The purpose of this study was to investigate the effect of platelet-derived growth factor (PDGF)-triggered signaling pathways and its downstream effectors in the migration of lens epithelial cells. Methods: In vitro scratch-wound healing and transwell migration assays were used to measure the migration of lens epithelial cells. The activation of PDGFR beta, phosphatidylinositol 3-kinas (PI3K)/protein kinase B (Akt) and mitogen activation protein kinase (MAPK) pathways, the impact of PDGF stimulation on the expression of cell protrusion molecules, and the stabilization of beta-catenin were measured by western blotting. The translocation of beta-catenin was detected using indirect immunofluorescence. Results: PDGF was found to enhance cell migration, which depended on the PI3K/Akt pathway. The activation of the PI3K/Akt pathway by the PDGF/PDGFR beta axis induced the up regulation of cell protrusion molecules and stabilization and translocation of beta-catenin, contributing to enhanced cell migration. Conclusion: Data from this study directly linked the central PI3K/Akt pathway to lens epithelial cell migration and pointed to new avenues for therapeutic intervention in PCO.
引用
收藏
页码：389 / 401
页数：13
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