EXPRESSION PATTERN OF M-CADHERIN IN NORMAL, DENERVATED, AND REGENERATING MOUSE MUSCLES

Citation
A. Irintchev et al., EXPRESSION PATTERN OF M-CADHERIN IN NORMAL, DENERVATED, AND REGENERATING MOUSE MUSCLES, Developmental dynamics, 199(4), 1994, pp. 326-337
Citations number
52
Categorie Soggetti
Developmental Biology","Anatomy & Morphology
Journal title
ISSN journal
10588388
Volume
199
Issue
4
Year of publication
1994
Pages
326 - 337
Database
ISI
SICI code
1058-8388(1994)199:4<326:EPOMIN>2.0.ZU;2-Y
Abstract
Following muscle damage in adult vertebrates, myofibers can be regener ated from muscle precursor cells (satellite cells). During this proces s, prenatal myogenesis is recapitulated to a large extent, both morpho logically and molecularly. A putative morphoregulatory molecule involv ed in myogenesis is M-cadherin (Mcad), a calcium-dependent cell adhesi on protein. The expression of Mead was studied by immunofluorescence i n regenerating, denervated, and normal mouse muscles. Our results demo nstrate that Mcad is present in satellite cells in normal muscle. Enha nced staining at sites of contact between satellite cells and the pare nt muscle fiber suggests an additional, spatially restricted expressio n of Mead in muscle fibers. Mcad positive cells in normal and denervat ed muscles did not incorporate bromodeoxyuridine within 24 hr after in jection in vivo, indicating that Mcad is expressed on mitotically quie scent satellite cells. Neural cell adhesion molecule (NCAM) co-localiz ed with Mcad in nearly all satellite cells in denervated muscles but r arely in intact muscles. At early stages of regeneration, Mcad was exc lusively and strongly expressed in myoblasts. After fusion of myoblast s into myotubes, Mcad was down-regulated and was barely detectable on more mature myotubes surrounded by distinct basal lamina sheaths. Thes e observations are in line with the idea that Mcad plays a crucial rol e in myogenesis. In intact muscle, Mcad might function as a molecular Link between satellite cell and muscle fiber. (C) 1994 Wiley-Liss, Inc .