Bex1 Participates in Muscle Regeneration by Regulating Myogenic Satellite Cell Differentiation.
10.5625/lar.2010.26.2.145
- Author:
Jae Hyung KOO
1
Author Information
1. Department of Anatomy and Neurobiology, School of Medicine, University of Maryland, Baltimore, USA. jkoo001@umaryland.edu
- Publication Type:Original Article
- Keywords:
Bex1;
calmodulin;
satellite cell;
muscle regeneration
- MeSH:
Animals;
Calmodulin;
Cell Cycle;
Cell Differentiation;
Cell Proliferation;
Cytoplasm;
Fluorescent Antibody Technique;
Mice;
Mice, Knockout;
Muscle Development;
Muscle Fibers, Skeletal;
Muscles;
Muscular Atrophy, Spinal;
Myoblasts;
Regeneration;
Satellite Cells, Skeletal Muscle
- From:Laboratory Animal Research
2010;26(2):145-151
- CountryRepublic of Korea
- Language:English
-
Abstract:
Bex1 protein is upregulated in regenerating muscle and interacts with calmodulin, a Ca2+-binding protein involved in cell cycle regulation. Following cardiotoxin-induced injury the regenerating muscle of Bex1 knock-out mice exhibits prolonged cell proliferation and delayed cell differentiation compared to wild-type mice. To gain insight into this process, we compared the regenerating myogenic morphologies of Bex1 knock-out and wild-type mice at several time points. Bex1-positive cells were identified by double immunofluorescence staining. These studies demonstrated that a population of cells that are Bex1-positive after injury are c-Met/basal lamina-positive and Mac-1-negative indicating that they are derived from at least a subset of myogenic progenitor/satellite cells but not invading immune cells. In addition, in regenerating muscle, Bex1 co-localizes with calmodulin in the cytoplasm of the late myoblast or early myotube stage of myogenesis. These results suggest that Bex1 participates in muscle regeneration through the regulation of satellite cell proliferation and differentiation by its interaction with calmodulin. Current studies of Bex1 may provide a new molecular tool for the identification of activated satellite cell and open the way to new or improved therapeutic regimens against progressive muscular atrophy.
