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

The Cardiovascular Institute and Departments of 1  Physiology and 2  Medicine, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois 60153 Proline-rich tyrosine kinase 2 (PYK2) is a member of the focal adhesion kinase (FAK) family of nonreceptor protein tyrosine kinases. PYK2 has...

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Published in:American journal of physiology. Heart and circulatory physiology 2002-08, Vol.283 (2), p.H695-H706
Main Authors: Bayer, Allison L, Heidkamp, Maria C, Patel, Nehu, Porter, Michael J, Engman, Steven J, Samarel, Allen M
Format: Article
Language:English
Subjects:
Adaptation, Physiological
Animals
Cardiac Output, Low - enzymology
Disease Progression
Focal Adhesion Kinase 1
Focal Adhesion Kinase 2
Focal Adhesion Protein-Tyrosine Kinases
Heart Ventricles
Hypertension - complications
Hypertrophy, Left Ventricular - enzymology
Hypertrophy, Left Ventricular - etiology
Hypertrophy, Left Ventricular - pathology
Male
Myocardium - enzymology
Myocardium - pathology
Phosphorylation
Protein-Tyrosine Kinases - metabolism
Rats
Rats, Sprague-Dawley
Tissue Distribution
Tyrosine - metabolism
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Summary:The Cardiovascular Institute and Departments of 1  Physiology and 2  Medicine, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois 60153 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  
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.00021.2002