Skeletal muscle cell activation by low-energy laser irradiation: A role for the MAPK/ERK pathway

Citation
G. Shefer et al., Skeletal muscle cell activation by low-energy laser irradiation: A role for the MAPK/ERK pathway, J CELL PHYS, 187(1), 2001, pp. 73-80
Citations number
51
Categorie Soggetti
Cell & Developmental Biology
Journal title
JOURNAL OF CELLULAR PHYSIOLOGY
ISSN journal
00219541 → ACNP
Volume
187
Issue
1
Year of publication
2001
Pages
73 - 80
Database
ISI
SICI code
0021-9541(200104)187:1<73:SMCABL>2.0.ZU;2-L
Abstract
Low-energy laser irradiation (LELI) has been shown to promote skeletal musc le regeneration in vivo and to activate skeletal muscle satellite cells, en hance their proliferation and inhibit differentiation in vitro. In the pres ent study, LELI, as well as the addition of serum to serum-starved myoblast s, restored their proliferation, whereas myogenic differentiation remained low. LELI induced mitogen-activated protein kinase/extracellular signal-reg ulated protein kinase (MAPK/ERK) phosphorylation with no effect on its expr ession in serum-starved myoblasts. Moreover, a specific MAPK kinase inhibit or (PD098059) inhibited the LELI- and 10% serum-mediated ERK1/2 activation. However, LELI did not affect jun N-terminal kinase (JNK) or p38 MAPK phosp horylation or protein expression. Whereas a 3-sec irradiation induced ERK1/ 2 phosphorylation, a 12-sec irradiation reduced it, again with no effect on JNK or p38. Moreover. LELI had distinct effects on receptor phosphorylatio n: it caused phosphorylation of the hepatocyte growth factor (HGF) receptor , previously shown to activate the MAPK/ERK pathway, whereas no effect was observed on tumor suppressor necrosis alpha (TNF-alpha) receptor which acti vates the p38 and JNK pathways. Therefore, by specifically activating MAPK/ ERK, but not INK and p38 MAPK enzymes, probably by specific receptor phosph orylation. LELI induces the activation and proliferation of quiescent satel lite cells and delays their differentiation. (C) 2001 Wiley-Liss Inc.