PMID- 10328964
OWN - NLM
STAT- MEDLINE
DCOM- 19990609
LR  - 20071114
IS  - 0014-4827 (Print)
IS  - 0014-4827 (Linking)
VI  - 249
IP  - 1
DP  - 1999 May 25
TI  - Tumor necrosis factor-alpha and basic fibroblast growth factor differentially 
      inhibit the insulin-like growth factor-I induced expression of myogenin in C2C12 
      myoblasts.
PG  - 177-87
AB  - Tumor necrosis factor-alpha (TNF-alpha) plays a role in several disease states 
      such as sepsis, cachexia, and non-insulin-dependent diabetes. TNF-alpha 
      interferes with insulin signaling and inhibits differentiation-specific gene 
      expression in adipose tissue and skeletal muscle. We have examined the mechanisms 
      by which TNF-alpha, in comparison to basic fibroblast growth factor (bFGF), 
      inhibits the insulin-like growth factor-I (IGF-I)-induced differentiation of 
      C2C12 myoblasts. Adhesion of quiescent, suspended myoblasts to collagen in high 
      concentrations of IGF-I (10 nM) induced these cells to proliferate during the 
      initial 24 h postplating and in so doing transiently inhibited the expression of 
      myogenin, an essential transcription factor controlling myoblast differentiation. 
      Low doses of IGF-I (1 nM) were minimally mitogenic and enhanced muscle-specific 
      gene expression. Quiescent myoblasts treated with bFGF in combination with IGF-I 
      did not express myogenin, but expressed proliferating cell nuclear antigen and 
      underwent DNA synthesis. In contrast, TNF-alpha in the presence or absence of 1 
      nM IGF-I, did not stimulate DNA synthesis in myoblasts. However, TNF-alpha 
      inhibited myogenin mRNA and protein expression. Expression of the 
      cyclin-dependent kinase inhibitor p21 correlated with myogenin expression and 
      myoblast differentiation, but not with growth arrest. These results indicate that 
      both TNF-alpha and bFGF inhibit myogenin expression but differentially influence 
      myoblast proliferation.
CI  - Copyright 1999 Academic Press.
FAU - Layne, M D
AU  - Layne MD
AD  - Department of Biochemistry, Boston University School of Medicine, Boston, 
      Massachusetts 02118, USA.
FAU - Farmer, S R
AU  - Farmer SR
LA  - eng
GR  - DK45058/DK/NIDDK NIH HHS/United States
GR  - HL07035/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (Myog protein, mouse)
RN  - 0 (Myogenin)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - 9007-34-5 (Collagen)
SB  - IM
MH  - Animals
MH  - Cell Adhesion
MH  - Cell Differentiation/drug effects
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - Collagen
MH  - Depression, Chemical
MH  - Fibroblast Growth Factor 2/*pharmacology
MH  - Gene Expression Regulation/*drug effects
MH  - Insulin-Like Growth Factor I/*antagonists & inhibitors/pharmacology
MH  - Mice
MH  - Muscle, Skeletal/cytology/*drug effects/metabolism
MH  - Myogenin/*biosynthesis/genetics
MH  - Phenotype
MH  - Transcription, Genetic/drug effects
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1999/05/18 00:00
MHDA- 1999/05/18 00:01
CRDT- 1999/05/18 00:00
PHST- 1999/05/18 00:00 [pubmed]
PHST- 1999/05/18 00:01 [medline]
PHST- 1999/05/18 00:00 [entrez]
AID - S0014-4827(99)94465-8 [pii]
AID - 10.1006/excr.1999.4465 [doi]
PST - ppublish
SO  - Exp Cell Res. 1999 May 25;249(1):177-87. doi: 10.1006/excr.1999.4465.