Linked Life Data

2162338

Source:http://linkedlifedata.com/resource/pubmed/id/2162338

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
1990-7-26
pubmed:abstractText
Transforming growth factor beta 1 (TGF-beta 1) is an inhibitor of skeletal muscle myoblast differentiation. Myoblast differentiation is dependent on the expression of certain myogenic differentiation genes and is affected by cell interaction with the extracellular matrix. We have searched for events in the differentiation process of L6E9 rat myoblasts that may be involved in the inhibitory action of TGF-beta 1. Elevated expression of the myogenic differentiation gene, myogenin, which is thought to play a central role in the differentiation process, occurs 10 h after the shift of L6E9 myoblasts to differentiation medium. Elevation of myogenin mRNA is blocked by TGF-beta 1 added at the time of the shift. This effect is preceded by, and might be related to, a rapid up-regulation of junB mRNA observed in TGF-beta 1-treated L6E9 myoblasts. However, TGF-beta 1 can also block myogenic differentiation in cells transfected with the myogenin gene under the control of a constitutive SV40 viral promoter. The nature of a mechanism that could mediate the inhibitory action of TGF-beta 1 without blocking myogenin mRNA expression is suggested by the observations that (a) TGF-beta 1 upregulates type I collagen expression and deposition in L6E9 myoblasts, (b) a fibrillar type I collagen layer inhibits L6E9 myoblast differentiation, and (c) inhibition of L6E9 myoblast differentiation by a type I collagen layer occurs without a block in myogenin expression. Thus, the data suggest that inhibition of L6E9 myoblast differentiation by TGF-beta 1 may be accomplished by at least two mechanisms acting in concert. One mechanism leads to a block in the expression of myogenin whereas the other mechanism may involve TGF-beta 1-induced changes in cell adhesion that either block the action of myogenic differentiation gene products or prevent the function of other as yet unknown components of the myogenic differentiation pathway.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
265
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10181-4
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:2162338-Animals, pubmed-meshheading:2162338-Cell Adhesion, pubmed-meshheading:2162338-Cell Differentiation, pubmed-meshheading:2162338-Cell Line, pubmed-meshheading:2162338-Collagen, pubmed-meshheading:2162338-DNA-Binding Proteins, pubmed-meshheading:2162338-Gene Expression Regulation, pubmed-meshheading:2162338-Kinetics, pubmed-meshheading:2162338-Muscle Proteins, pubmed-meshheading:2162338-Muscles, pubmed-meshheading:2162338-Myogenin, pubmed-meshheading:2162338-Protein-Tyrosine Kinases, pubmed-meshheading:2162338-Proto-Oncogene Proteins, pubmed-meshheading:2162338-Proto-Oncogene Proteins c-jun, pubmed-meshheading:2162338-RNA, Messenger, pubmed-meshheading:2162338-Rats, pubmed-meshheading:2162338-Transcription, Genetic, pubmed-meshheading:2162338-Transcription Factors, pubmed-meshheading:2162338-Transforming Growth Factors
pubmed:year
1990
pubmed:articleTitle
Cell adhesion to collagen and decreased myogenic gene expression implicated in the control of myogenesis by transforming growth factor beta.
pubmed:affiliation
Cell Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.