Objective: To investigate the role of focal adhesion kinase (FAK) in cardiac hypertrophy induced by hypertension. Methods: 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. Results: 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. Conclusion: Phosphorylation and translocation of serine 722 and serine 910 of phosphorylated FAK play an important role in the de-compensatory cardiac hypertrophy.
|Original language||English (US)|
|Number of pages||5|
|Journal||Chinese Journal of Pathology|
|State||Published - May 2008|
- Focal adhesion kinase 1
- Models, animal
- Signaling transduction