|  Help  |  About  |  Contact Us

Publication : α-Syntrophin is required for the hepatocyte growth factor-induced migration of cultured myoblasts.

First Author  Kim MJ Year  2011
Journal  Exp Cell Res Volume  317
Issue  20 Pages  2914-24
PubMed ID  22001117 Mgi Jnum  J:178524
Mgi Id  MGI:5299242 Doi  10.1016/j.yexcr.2011.09.017
Citation  Kim MJ, et al. (2011) alpha-Syntrophin is required for the hepatocyte growth factor-induced migration of cultured myoblasts. Exp Cell Res 317(20):2914-24
abstractText  Syntrophins are adaptor proteins that link intracellular signaling molecules to the dystrophin based scaffold. In this study, we investigated the function of syntrophins in cell migration, one of the early steps in myogenic differentiation and in regeneration of adult muscle. Hepatocyte growth factor (HGF) stimulates migration and lamellipodia formation in cultured C2 myoblasts. In the migrating cells, syntrophin concentrated in the rear-lateral region of the cell, opposite of the lamellipodia, instead of being diffusely present throughout the cytoplasm of non-migrating cells. When the expression of alpha-syntrophin, the major syntrophin isoform of skeletal muscle, was reduced by transfection with the alpha-syntrophin-specific siRNA, HGF stimulation of lamellipodia formation was prevented. Likewise, migration of myoblasts from alpha-syntrophin knockout mice could not be stimulated by HGF. However, HGF-induced migration was restored in myoblasts isolated from a transgenic mouse expressing alpha-syntrophin only in muscle cells. Treatment of C2 myoblasts with inhibitors of PI3-kinase not only reduced the rate of cell migration, but also impaired the accumulation of syntrophins in the rear-lateral region of the migrating cells. Phosphorylation of Akt was reduced in the alpha-syntrophin siRNA-treated C2 cells. These results suggest that alpha-syntrophin is required for HGF-induced migration of myoblasts and for proper PI3-kinase/Akt signaling.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

6 Bio Entities

Trail: Publication

0 Expression