Document Detail

Cardiac-specific LIM protein FHL2 modifies the hypertrophic response to beta-adrenergic stimulation.
MedLine Citation:
PMID:  11390345     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: A deficiency of muscle LIM protein results in dilated cardiomyopathy, but the function of other LIM proteins in the heart has not been assessed previously. We have characterized the expression and function of FHL2, a heart-specific member of the LIM domain gene family. METHODS AND RESULTS: Expression of FHL2 mRNA and protein was examined by Northern blot, in situ hybridization, and Western blot analyses of fetal and adult mice. FHL2 transcripts are present at embryonic day (E) 7.5 within the cardiac crescent in a pattern that resembles that of Nkx2.5 mRNA. During later stages of cardiac development and in adult animals, FHL2 expression is localized to the myocardium and absent from endocardium, cardiac cushion, outflow tract, or coronary vasculature. The gene encoding FHL2 was disrupted by homologous recombination, and knockout mice devoid of FHL2 were found to undergo normal cardiovascular development. In the absence of FHL2, however, cardiac hypertrophy resulting from chronic infusion of isoproterenol is exaggerated (59% versus 20% increase in heart weight/body weight in FHL null versus wild-type mice; P<0.01). CONCLUSIONS: FHL2 is an early marker of cardiogenic cells and a cardiac-specific LIM protein in the adult. FHL2 is not required for normal cardiac development but modifies the hypertrophic response to beta-adrenergic stimulation.
Y Kong; J M Shelton; B Rothermel; X Li; J A Richardson; R Bassel-Duby; R S Williams
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  103     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2001 Jun 
Date Detail:
Created Date:  2001-06-06     Completed Date:  2001-07-12     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2731-8     Citation Subset:  AIM; IM    
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-8573, USA.
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MeSH Terms
Adrenergic beta-Agonists / pharmacology*
Amino Acid Sequence
Blotting, Northern
Embryo, Mammalian / metabolism
Gene Expression
Gene Expression Regulation, Developmental
Homeodomain Proteins / genetics,  physiology*
Hypertrophy / chemically induced,  genetics
In Situ Hybridization
Isoproterenol / pharmacology
Mice, Inbred Strains
Mice, Knockout
Molecular Sequence Data
Muscle Proteins*
Myocardium / metabolism*,  pathology
RNA, Messenger / genetics,  metabolism
Recombinant Fusion Proteins / genetics,  metabolism
Sequence Alignment
Sequence Homology, Amino Acid
Tissue Distribution
Transcription Factors*
Xenopus Proteins*
beta-Galactosidase / genetics,  metabolism
Grant Support
Reg. No./Substance:
0/Adrenergic beta-Agonists; 0/FHL2 protein, human; 0/Fhl2 protein, mouse; 0/Homeodomain Proteins; 0/Muscle Proteins; 0/NKX2-5 protein, human; 0/Nkx2-5 protein, mouse; 0/RNA, Messenger; 0/Recombinant Fusion Proteins; 0/Transcription Factors; 0/Xenopus Proteins; 7683-59-2/Isoproterenol; EC

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