Document Detail


Insulin-like growth factor-induced transcriptional activity of the skeletal alpha-actin gene is regulated by signaling mechanisms linked to voltage-gated calcium channels during myoblast differentiation.
MedLine Citation:
PMID:  14684598     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
IGF-I activates signaling pathways that increase the expression of muscle-specific genes in differentiating myoblasts. Induction of skeletal alpha-actin expression occurs during differentiation through unknown mechanisms. The purpose of this investigation was to examine the mechanisms that IGF-I uses to induce skeletal alpha-actin gene expression in C2C12 myoblasts. IGF-I increased skeletal alpha-actin promoter activity by 107% compared with the control condition. Ni(+) [T-type voltage-gated Ca(2+) channel (VGCC) inhibitor] reduced basal-induced activation of the skeletal alpha-actin promoter by approximately 84%, and nifedipine (L-type VGCC inhibitor) inhibited IGF-I-induced activation of the skeletal alpha-actin promoter by 29-48%. IGF-I failed to increase skeletal alpha-actin promoter activity in differentiating dysgenic (lack functional L-type VGCC) myoblasts; 30 mm K(+) and 30 mm K(+)+IGF-I increased skeletal alpha-actin promoter activity by 162% and 76% compared with non-IGF-I or IGF-I-only conditions, respectively. IGF-I increased calcineurin activity, which was inhibited by cyclosporine A. Further, cyclosporine A inhibited K(+)+IGF-I-induced activation of the skeletal alpha-actin promoter. Constitutively active calcineurin increased skeletal alpha-actin promoter activity by 154% and rescued the nifedipine-induced inhibition of L-type VGCC but failed to rescue the Ni(+)-inhibition of T-type VGCC. IGF-I-induced nuclear factor of activated T-cells transcriptional activity was not inhibited by nifedipine or Ni(+). IGF-I failed to increase serum response factor transcriptional activity; however, serum response factor activity was reduced in the presence of Ni(+). These data suggest that IGF-I-induced activation of the skeletal alpha-actin promoter is regulated by the L-type VGCC and calcineurin but independent of nuclear factor of activated T-cell transcriptional activity as C2C12 myoblasts differentiate into myotubes.
Authors:
Espen E Spangenburg; Douglas K Bowles; Frank W Booth
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2003-12-18
Journal Detail:
Title:  Endocrinology     Volume:  145     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  2004 Apr 
Date Detail:
Created Date:  2004-03-17     Completed Date:  2004-04-16     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2054-63     Citation Subset:  AIM; IM    
Affiliation:
Department of Biomedical Sciences, University of Missouri, Columbia 65211, USA. eespangenburg@ucdavis.edu
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MeSH Terms
Descriptor/Qualifier:
Actins / genetics*
Animals
Bone and Bones / metabolism*
Calcineurin / physiology
Calcium Channels / metabolism*,  physiology
Cell Differentiation
Cell Line
Humans
Insulin-Like Growth Factor I / pharmacology,  physiology*
Mice
Myoblasts / cytology*
Promoter Regions, Genetic / drug effects,  physiology
Recombinant Proteins / pharmacology
Serum Response Factor / genetics
Signal Transduction / physiology*
Transcription, Genetic / drug effects,  physiology*
Grant Support
ID/Acronym/Agency:
AR19393/AR/NIAMS NIH HHS; AR48514/AR/NIAMS NIH HHS; HL52940/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Actins; 0/Calcium Channels; 0/Recombinant Proteins; 0/Serum Response Factor; 67763-96-6/Insulin-Like Growth Factor I; EC 3.1.3.16/Calcineurin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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