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Cardiac-specific LIM protein FHL2 modifies the hypertrophic response to beta-adrenergic stimulation.

Publication ,  Journal Article
Kong, Y; Shelton, JM; Rothermel, B; Li, X; Richardson, JA; Bassel-Duby, R; Williams, RS
Published in: Circulation
June 5, 2001

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.

Duke Scholars

Published In

Circulation

DOI

EISSN

1524-4539

Publication Date

June 5, 2001

Volume

103

Issue

22

Start / End Page

2731 / 2738

Location

United States

Related Subject Headings

  • beta-Galactosidase
  • Xenopus Proteins
  • Transcription Factors
  • Tissue Distribution
  • Sequence Homology, Amino Acid
  • Sequence Alignment
  • Recombinant Fusion Proteins
  • RNA, Messenger
  • Myocardium
  • Muscle Proteins
 

Citation

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Kong, Y., Shelton, J. M., Rothermel, B., Li, X., Richardson, J. A., Bassel-Duby, R., & Williams, R. S. (2001). Cardiac-specific LIM protein FHL2 modifies the hypertrophic response to beta-adrenergic stimulation. Circulation, 103(22), 2731–2738. https://doi.org/10.1161/01.cir.103.22.2731
Kong, Y., J. M. Shelton, B. Rothermel, X. Li, J. A. Richardson, R. Bassel-Duby, and R. S. Williams. “Cardiac-specific LIM protein FHL2 modifies the hypertrophic response to beta-adrenergic stimulation.Circulation 103, no. 22 (June 5, 2001): 2731–38. https://doi.org/10.1161/01.cir.103.22.2731.
Kong Y, Shelton JM, Rothermel B, Li X, Richardson JA, Bassel-Duby R, et al. Cardiac-specific LIM protein FHL2 modifies the hypertrophic response to beta-adrenergic stimulation. Circulation. 2001 Jun 5;103(22):2731–8.
Kong, Y., et al. “Cardiac-specific LIM protein FHL2 modifies the hypertrophic response to beta-adrenergic stimulation.Circulation, vol. 103, no. 22, June 2001, pp. 2731–38. Pubmed, doi:10.1161/01.cir.103.22.2731.
Kong Y, Shelton JM, Rothermel B, Li X, Richardson JA, Bassel-Duby R, Williams RS. Cardiac-specific LIM protein FHL2 modifies the hypertrophic response to beta-adrenergic stimulation. Circulation. 2001 Jun 5;103(22):2731–2738.

Published In

Circulation

DOI

EISSN

1524-4539

Publication Date

June 5, 2001

Volume

103

Issue

22

Start / End Page

2731 / 2738

Location

United States

Related Subject Headings

  • beta-Galactosidase
  • Xenopus Proteins
  • Transcription Factors
  • Tissue Distribution
  • Sequence Homology, Amino Acid
  • Sequence Alignment
  • Recombinant Fusion Proteins
  • RNA, Messenger
  • Myocardium
  • Muscle Proteins