Linked Life Data

16682418

Source:http://linkedlifedata.com/resource/pubmed/id/16682418

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
27
pubmed:dateCreated
2006-7-3
pubmed:abstractText
Transforming growth factor (TGF-beta) is involved in several cellular processes such as cell proliferation, differentiation, and apoptosis. At the cell surface, TGF-beta binds to serine-threonine kinase transmembrane receptors (type II and type I) to initiate Smad-dependent intracellular signaling cascades. During the early stages of skeletal muscle differentiation, myotubes start to evoke spontaneous electrical activity in association with contractions that arise following the maturation of the excitation-contraction apparatus. In this work, we report that TGF-beta-dependent signaling is regulated by electrical activity in developing rat primary myotubes, as determined by Smad2 phosphorylation, Smad4 nuclear translocation, and p3TPLux reporter activity. This electrical activity-dependent regulation is associated with changes in TGF-beta type I receptor (TbetaRI) levels, correlated with changes in transducing receptors at the cell membrane (measured through radiolabeling binding assays). The inhibition of electrical activity with tetrodotoxin, a voltage-dependent sodium channel blocker, increases TbetaRI levels via a transcription-dependent mechanism. In contrast, the promotion of electrical activity in myotube cultures, induced by the up-regulation of voltage-dependent sodium channels or by direct stimulation with extracellular electrodes, causes TbetaRI levels to decrease. Similar results were obtained in denervated adult muscles, suggesting that electrical activity-dependent regulation of TbetaRI also occurs in vivo. Additional results suggest that this activity-dependent regulation is mediated by myogenin. Altogether, these findings support the possibility for a novel regulatory mechanism acting on TGF-beta signaling cascade in skeletal muscle cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
281
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
18473-81
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16682418-Activin Receptors, Type I, pubmed-meshheading:16682418-Animals, pubmed-meshheading:16682418-Electric Stimulation, pubmed-meshheading:16682418-Gene Expression Regulation, pubmed-meshheading:16682418-Male, pubmed-meshheading:16682418-Muscle, Skeletal, pubmed-meshheading:16682418-Muscle Contraction, pubmed-meshheading:16682418-Muscle Fibers, Skeletal, pubmed-meshheading:16682418-Phosphorylation, pubmed-meshheading:16682418-Protein-Serine-Threonine Kinases, pubmed-meshheading:16682418-Rats, pubmed-meshheading:16682418-Rats, Sprague-Dawley, pubmed-meshheading:16682418-Receptors, Transforming Growth Factor beta, pubmed-meshheading:16682418-Signal Transduction, pubmed-meshheading:16682418-Smad2 Protein, pubmed-meshheading:16682418-Smad4 Protein, pubmed-meshheading:16682418-Transcriptional Activation, pubmed-meshheading:16682418-Transforming Growth Factor beta
pubmed:year
2006
pubmed:articleTitle
Transforming growth factor beta (TGF-beta) signaling is regulated by electrical activity in skeletal muscle cells. TGF-beta type I receptor is transcriptionally regulated by myotube excitability.
pubmed:affiliation
Centro de Regulación Celular y Patología Joaquín V. Luco, Millennium Institute for Fundamental and Applied Biology, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago, Chile.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't