高血压大鼠左心室肥大心肌细胞中黏着斑激酶丝氨酸722和910磷酸化及其核转位  

Phosphorylation and nuclear translocation of serine 722 and serine 910 of focal adhesion kinase in hypertrophic cardiac myocytes of left ventricle of spontaneously hypertensive rats

作　　者：钟玲[1] 易先平[1] 李展宇[1] Faqian Li 

机构地区：[1]中山大学附属第五医院病理科,珠海519000 [2]South Dakota Health Research Foundation Cardiovascular Research Institute, University of South Dakota, SiouxFalls, SD, USA

出　　处：《中华病理学杂志》2008年第5期328-332,共5页Chinese Journal of Pathology

基　　金：国家自然科学基金资助项目（30470696）;珠海市科技计划项目（PB20075024）

摘　　要：目的 探讨黏着斑激酶（FAK）在高血压致左心室肥大发生发展过程中的作用。方法以特发性高血压心力衰竭（SHHF）大白鼠为研究对象，通过免疫荧光标记、共聚焦显微镜及Western blot等方法，检测不同月龄SHHF大白鼠左心室心肌细胞中丝氨酸722磷酸化的FAK（FAK-pSer722）和丝氨酸910磷酸化的FAK（FAK-pSer910）的表达与分布。结果 2月龄时SHHF组与对照组比较，FAK-pSer722和FAK-pSer910表达无明显区别，在6、12和18月龄时SHHF组FAK-pSer722和FAK-pSer910表达均明显增加并表现出明显核内聚积。结论 在心肌失代偿肥大的发生发展过程中，存在着FAK丝氨酸722和丝氨酸910两位点的磷酸化增加和核内聚积，与心肌纤维的纵向性生长的过程相吻合，而与早期心肌向心性肥大无关。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-pSerg10 expression between 2 month- old SHHF and WKY rats. In contrast with the control groups, the expression of FAK-pSer722 and FAK- pSerg10 significantly increased in cardiac myocytes of the left ventricle, from 6, 12 and 18 month-old SHHF rats. Both FAK-pSer722 and FAK-pSergl0 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.

关 键 词：黏着斑激酶1 高血压 信号传导 模型 动物 

分 类 号：R686[医药卫生—骨科学]