Insulin promotes proliferation of skeletal myoblast cells through PI3K/Akt and MEK/ERK pathways in rats.
- Author:
Huan YU
1
;
Min ZHANG
;
Yong ZHAO
;
Ping WU
;
Pei-Liang CHEN
;
Wei-Dong LI
Author Information
1. The Systems Bio-medicine Key Laboratory of Jiangxi, Jiujiang University, China.
- Publication Type:Journal Article
- MeSH:
Androstadienes;
pharmacology;
Animals;
Butadienes;
pharmacology;
Cell Proliferation;
Cells, Cultured;
Enzyme Inhibitors;
pharmacology;
Insulin;
pharmacology;
MAP Kinase Signaling System;
Myoblasts, Skeletal;
cytology;
drug effects;
Nitriles;
pharmacology;
Phosphatidylinositol 3-Kinases;
metabolism;
Phosphorylation;
Proto-Oncogene Proteins c-akt;
metabolism;
Rats
- From:
Acta Physiologica Sinica
2013;65(1):19-25
- CountryChina
- Language:Chinese
-
Abstract:
The present study was to explore the effects of insulin on proliferation of skeletal myoblast cells in rats. Separated and cultured primary skeletal myoblast cells from rats were treated by insulin. By means of the incorporation of (3)H-TdR, BrdU assay and MTT assay, the proliferation of skeletal myoblast cells was detected. Western blot was used to check the phosphorylation of Akt and ERK of myoblast cells. The results showed that insulin significantly promoted the incorporation of (3)H-TdR into cultured skeletal myoblast cells in a dose-dependent manner. MTT assay and BrdU assay also showed insulin promoted the proliferation of skeletal myoblast cells. The promotion of skeletal myoblast cells proliferation by insulin was inhibited by PI3K inhibitor wortmannin or MEK inhibitor U0126, and the same phenomenon was shown in L6 and C2C12 cells. Also, insulin increased the phosphorylation of Akt and ERK in myoblast cells. These results suggest that insulin may promote proliferation of skeletal myoblast cells through PI3K/Akt and MEK/ERK pathways.
