Expression of focal adhesion kinase in cardiac myocytes of hypertrophic ventricle.
- Author:
Zhan-yu LI
1
;
Xian-ping YI
;
Ling ZHONG
;
Fa-qian LI
;
Wen-ying ZHOU
;
Wan-wei CAO
;
Yan-xuan ZHENG
;
Xiao-hong WANG
;
Ya-nan WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Focal Adhesion Kinase 1; metabolism; Heart Ventricles; pathology; Hypertension; complications; Hypertrophy, Left Ventricular; enzymology; etiology; Male; Microscopy, Confocal; Myocytes, Cardiac; metabolism; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Signal Transduction
- From: Chinese Journal of Pathology 2007;36(10):677-680
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVESTo investigate the role of focal adhesion kinase (FAK) in the pathogenesis of cardiac hypertrophy induced by hypertension.
METHODSUsing 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.
RESULTSThere 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.
CONCLUSIONSFAK may play a role in the cell signaling transduction leading to cardiac hypertrophy, presumably through regulations of hypertrophic gene transcription and RNA processing.
