Striated muscle-specific beta(1D)-integrin and FAK are involved in cardiac myocyte hypertrophic response pathway.

@article{Pham2000StriatedMB,
  title={Striated muscle-specific beta(1D)-integrin and FAK are involved in cardiac myocyte hypertrophic response pathway.},
  author={Can G. Pham and Alice E Harpf and Rebecca S. Keller and Hien Thi Vu and Shaw Yung Shai and Joseph C. Loftus and Robert S. Ross},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2000},
  volume={279 6},
  pages={
          H2916-26
        }
}
  • C. Pham, A. Harpf, +4 authors R. Ross
  • Published 1 December 2000
  • Biology
  • American journal of physiology. Heart and circulatory physiology
Alterations in the extracellular matrix occur during the cardiac hypertrophic process. Because integrins mediate cell-matrix adhesion and beta(1D)-integrin (beta1D) is expressed exclusively in cardiac and skeletal muscle, we hypothesized that beta1D and focal adhesion kinase (FAK), a proximal integrin-signaling molecule, are involved in cardiac growth. With the use of cultured ventricular myocytes and myocardial tissue, we found the following: 1) beta1D protein expression was upregulated… 

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References

SHOWING 1-10 OF 79 REFERENCES
Beta1 integrins participate in the hypertrophic response of rat ventricular myocytes.
TLDR
Findings show that integrin ligation and signaling are involved in the cardiac hypertrophic response pathway.
β1 Integrins Participate in the Hypertrophic Response of Rat Ventricular Myocytes
TLDR
The hypothesis that β1 integrin function is involved in the α1-adrenergic mediated hypertrophic response of neonatal rat ventricular myocytes was evaluated and specificity of results was confirmed by demonstrating that ventricularMyocytes plated onto an anti–β1 Integrin antibody supported the hypertrophic gene response.
Endothelin-induced cardiac myocyte hypertrophy: role for focal adhesion kinase.
TLDR
Although FAK is necessary for ET-induced NRVM hypertrophy, other ET-generated signals are also required to elicit the hypertrophic phenotype.
Differentiation and integrity of cardiac muscle cells are impaired in the absence of beta 1 integrin.
TLDR
It is concluded that interactions with the extracellular matrix via beta 1 integrin is necessary for differentiation and the maintenance of a specialized phenotype of cardiac muscle cells.
Expression of collagen binding integrins during cardiac development and hypertrophy.
TLDR
The present immunohistochemical, cell adhesion, and biochemical data clearly indicate that integrins play a major role in the regulation of the interaction between cardiac myocytes and the extracellular matrix during development and disease.
A Role for the p38 Mitogen-activated Protein Kinase Pathway in Myocardial Cell Growth, Sarcomeric Organization, and Cardiac-specific Gene Expression
TLDR
Novel and potentially central roles for MKK6 and p38 in the regulation of myocardial cell hypertrophy are demonstrated.
Outside-in signalling of fibronectin stimulates cardiomyocyte hypertrophy in cultured neonatal rat ventricular myocytes.
TLDR
The interaction of fibronectin and RGD-dependent integrins is involved in the hypertrophic responses of myocyte in vitro, and this work suggests that extracellular matrix proteins such as fibronECTin are not merely passive adhesive molecules but are active participants in processes leading to myocyte hypertrophy.
Oncogenic src, raf, and rasStimulate a Hypertrophic Pattern of Gene Expression and Increase Cell Size in Neonatal Rat Ventricular Myocytes*
TLDR
It is concluded that members of the Src family of tyrosine kinases may be important in mediating the transcriptional changes occurring during cardiac myocyte hypertrophy and that Ras and Raf may be downstream effectors.
β1D Integrin Inhibits Cell Cycle Progression in Normal Myoblasts and Fibroblasts*
TLDR
Exogenous expression of the exogenous β1D integrin in C2C12 myoblasts and NIH 3T3 or REF 52 fibroblasts inhibited cell proliferation and showed a new specific function for the alternatively spliced β1d integrin isoform.
Fibronectin expression during physiological and pathological cardiac growth.
...
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2
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4
5
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