ABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of focal adhesion kinase (FAK) in cardiac hypertrophy induced by hypertension.</p><p><b>METHODS</b>Using immunofluorescent labeling, confocal microscopy and Western blot, the expression and subcellular location of FAK-pSer722 and FAK-pSer910 were determined in cardiac myocytes of the left ventricles from 2, 6, 12, and 18 month-old spontaneously hypertensive heart failure (SHHF) rats and age-matched Wistar-Kyoto (WKY) control rats, respectively.</p><p><b>RESULTS</b>There was no obvious difference in FAK-pSer722 and FAK-pSer910 expression between 2 month-old SHHF and WKY rats. In contrast with the control groups, the expression of FAK-pSer722 and FAK-pSer910 significantly increased in cardiac myocytes of the left ventricle, from 6, 12 and 18 month-old SHHF rats. Both FAK-pSer722 and FAK-pSer910 were translocated and acummulated in nuclei of cardiac myocytes from 6, 12, and 18 month-old SHHF rats.</p><p><b>CONCLUSION</b>Phosphorylation and translocation of serine 722 and serine 910 of phosphorylated FAK play an important role in the de-compensatory cardiac hypertrophy.</p>
Subject(s)
Animals , Rats , Cardiomegaly , Metabolism , Cell Nucleus , Metabolism , Focal Adhesion Kinase 1 , Metabolism , Focal Adhesion Protein-Tyrosine Kinases , Metabolism , Physiology , Heart Failure , Heart Ventricles , Pathology , Hypertension , Hypertrophy , Myocytes, Cardiac , Pathology , Phosphorylation , Protein Transport , Physiology , Rats, Inbred SHR , Rats, Inbred WKY , Serine , Metabolism , Signal Transduction , PhysiologyABSTRACT
<p><b>OBJECTIVES</b>To investigate the role of focal adhesion kinase (FAK) in the pathogenesis of cardiac hypertrophy induced by hypertension.</p><p><b>METHODS</b>Using immunofluorescent labeling, confocal microscopy and Western blotting, the expression and subcellular localization of FAK in the cardiac myocytes of left ventricle were determined in 2, 6, 12, and 18 month-old rats with spontaneously hypertensive heart failure (SHHF) along with age-matched control Wistar-Kyoto (WKY) rats.</p><p><b>RESULTS</b>There was no significant difference of FAK expression between 2 month-old SHHF and WKY rats (50.5+/-6.9 vs. 49.8+/-5.0, n=6, P>0.05). In contrast with the control groups, the expression of FAK significantly increased in 6, 12 and 18 month-old SHHF rats (130.6+/-3.0 vs. 47.3+/-1.3, 144.7+/-5.4 vs. 46.4+/-3.1, 141.4+/-9.8 vs. 48.5+/-2.2, each groups n=6, P<0.05) with FAK protein primarily cumulated in the intercalated disks and nuclei.</p><p><b>CONCLUSIONS</b>FAK may play a role in the cell signaling transduction leading to cardiac hypertrophy, presumably through regulations of hypertrophic gene transcription and RNA processing.</p>