PYK2 expression and phosphorylation increases in pressure overload-induced left ventricular hypertrophy

Allison L Bayer, Maria C. Heidkamp, Nehu Patel, Michael J. Porter, Steven J. Engman, Allen M. Samarel

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Proline-rich tyrosine kinase 2 (PYK2) is a member of the focal adhesion kinase (FAK) family of nonreceptor protein tyrosine kinases. PYK2 has been implicated in linking G protein-coupled receptors to activation of mitogen-activated protein kinase cascades and cellular growth in a variety of cell types. To determine whether PYK2 expression and phosphorylation is altered in left ventricular (LV) myocardium undergoing LV hypertrophy (LVH) and heart failure in vivo, suprarenal abdominal aortic coarctation was performed in 160-g male Sprague-Dawley rats. Immunohistochemistry and Western blotting were performed on LV tissue 1, 8, and 24 wk after aortic banding. Aortic banding produced sustained hypertension and gradually developing LVH. PYK2 levels were increased 1.8 ± 0.2-, 2.7 ± 0.6-, and 2.0 ± 0.2-fold in 1-, 8-, and 24-wk banded animals compared with their respective sham-operated controls. The increase in PYK2 expression was paralleled by an increase in PYK2 phosphorylation, both of which preceded the development of LVH. Immunohistochemistry revealed that enhanced PYK2 expression occurred predominantly in the cardiomyocyte population. Furthermore, there was a high degree of correlation (R = 0.75; P < 0.001) between the level of PYK2 and the degree of LVH in 24-wk sham and banded animals. In contrast, FAK levels and FAK phosphorylation were not increased before the development of LVH. However, there was a high degree of correlation (R = 0.68; P < 0.001) between the level of FAK and the degree of LVH in 24-wk sham and banded rats. There was also a significant increase in the ratio of phosphospecific anti-FAK to FAK at this time point. These data are consistent with a role for PYK2 in the induction of pressure overload-induced cardiomyocyte hypertrophy, and suggest that PYK2 and FAK have distinctly different roles in LVH progression.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume283
Issue number2 52-2
StatePublished - Jul 30 2002
Externally publishedYes

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Focal Adhesion Kinase 2
Left Ventricular Hypertrophy
Focal Adhesion Protein-Tyrosine Kinases
Phosphorylation
Pressure
Hypertrophy
Cardiac Myocytes
Immunohistochemistry
Aortic Coarctation
G-Protein-Coupled Receptors
Mitogen-Activated Protein Kinases
Protein-Tyrosine Kinases
Sprague Dawley Rats
Myocardium

Keywords

  • Cytoskeleton
  • Focal adhesion kinase
  • Heart failure
  • Signal transduction

ASJC Scopus subject areas

  • Physiology

Cite this

PYK2 expression and phosphorylation increases in pressure overload-induced left ventricular hypertrophy. / Bayer, Allison L; Heidkamp, Maria C.; Patel, Nehu; Porter, Michael J.; Engman, Steven J.; Samarel, Allen M.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 283, No. 2 52-2, 30.07.2002.

Research output: Contribution to journalArticle

Bayer, Allison L ; Heidkamp, Maria C. ; Patel, Nehu ; Porter, Michael J. ; Engman, Steven J. ; Samarel, Allen M. / PYK2 expression and phosphorylation increases in pressure overload-induced left ventricular hypertrophy. In: American Journal of Physiology - Heart and Circulatory Physiology. 2002 ; Vol. 283, No. 2 52-2.
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AU - Samarel, Allen M.

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