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Articles in PresS, published online ahead of print April 25, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00021.2002
Submitted on January 14, 2002
Accepted on April 20, 2002
1 Cardiovascular Institute, Loyola University Chicago Stritch School of Medicine, Maywood, IL, USA; Physiology, Loyola University Chicago Stritch School of Medicine, Maywood, IL, USA
2 Cardiovascular Institute, Loyola University Chicago Stritch School of Medicine, Maywood, IL, USA; Medicine, Loyola University Chicago Stritch School of Medicine, Maywood, IL, USA
3 Cardiovascular Institute, Loyola University Chicago Stritch School of Medicine, Maywood, IL, USA; Physiology, Loyola University Chicago Stritch School of Medicine, Maywood, IL, USA; Medicine, Loyola University Chicago Stritch School of Medicine, Maywood, IL, USA
* To whom correspondence should be addressed. E-mail: asamare{at}lumc.edu.
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 (MAPK) cascades and cellular growth in a variety of cell types. To determine whether PYK2 expression and phosphorylation is altered in left ventricular myocardium undergoing hypertrophy (LVH) and heart failure in vivo, suprarenal abdominal aortic coarctation was performed in 160g, male Sprague-Dawley rats. Immunohistochemistry and Western blotting were performed on LV tissue 1, 8 and 24 weeks (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 1wk-, 8wk-, 24wk-banded animals as compared to 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 24wk-sham and banded animals. In contrast, FAK levels and FAK phosphorylation were not increased prior to 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 24wk-sham and banded rats. There was also a significant increase in the ratio of pFAK 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.
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