PTEN silencing enhances neuronal proliferation and differentiation by activating PI3K/Akt/GSK3β pathway in vitro

被引:27
|
作者
Song, Zhiwen [1 ]
Han, Xiu [2 ]
Shen, Liming [1 ]
Zou, Hongjun [1 ]
Zhang, Bin [3 ]
Liu, Jinbo [1 ]
Gong, Aihua [2 ]
机构
[1] Soochow Univ, Dept Orthoped, Affiliated Hosp 3, Changzhou 213003, Peoples R China
[2] Jiangsu Univ, Sch Med, Dept Cell Biol, Zhenjiang 212013, Peoples R China
[3] Jining Med Univ, Affiliated Hosp, Dept Lab Med, Jining 272000, Peoples R China
基金
中国国家自然科学基金;
关键词
PTEN; PI3K/Akt/GSK3 beta pathway; Neuronal cells; Proliferation; Differentiation; SPINAL-CORD-INJURY; AXON REGENERATION; CELL-PROLIFERATION; NEURITE OUTGROWTH; SIGNALING PATHWAY; PC12; CELLS; DELETION; MICE; INHIBITION; WNT;
D O I
10.1016/j.yexcr.2018.01.001
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The failure of neuronal proliferation and differentiation is a major obstacle for neural repair and regeneration after traumatic central nervous system (CNS) injury. PTEN acts as an intrinsic brake on the neuronal cells, but its roles and mechanism still remain to be clarified. Herein, for the first time we confirmed that PTEN had a dual effect on the neuronal cells in vitro. Firstly, we found that PTEN knockdown significantly promoted cell proliferation and differentiation. Then, PTEN knockdown activated PI3K/Akt and Wnt/beta-catenin pathways in vitro. Further evidence revealed that GSK3 beta as a key node involved in PTEN controlling cell proliferation and differentiation in PC12 cells. In addition, we identified that PTEN-GSK3 beta pathway modulated neuronal proliferation via beta-catenin. Taken together, these results suggest that PTEN silencing enhances neuronal proliferation and differentiation by activating PI3K/Akt/GSK3 beta pathway that it may be a promising therapeutic approach for CNS injury.
引用
收藏
页码:179 / 187
页数:9
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