摘要
目的:探讨人心室肥厚时心肌酪氨酸(Janus)激酶/信号转导子/转录激活子(JAKsSTATs)基因表达的改变及意义。方法:应用病理检查、放射免疫和蛋白印迹杂交等方法,比较心肌肥厚患者(心肌肥厚组)和正常人(对照组)心肌细胞直径、心肌间质胶原容积分数和心肌血管周围胶原面积、心脏局部血管紧张素II(Ang II)水平和心脏JAK1,2及STAT1,3蛋白表达差异。结果:心肌肥厚组心肌细胞直径、心肌间质胶原容积分数和心肌血管周围胶原面积比均明显比对照组增高(均P<0.01)。心肌肥厚组心肌组织匀浆液Ang II水平为(179.3±36.1)pg/mg心肌组织,对照组为(103.2±13.6)pg/mg心肌组织,与对照组比较,心肌肥厚组心肌组织Ang II水平明显增高(P<0.01)。心肌肥厚组心肌组织JAK1,2及STAT1,3蛋白表达明显增加(均P<0.01)。结论:JAKs-STATs信号通路可能参与了心肌细胞肥大和心肌纤维化过程。
Objective： To evaluate the role of Janus kinases-signal transducers and activators of transcription（ JAKs-STATs） in patients with myocardial hypertrophy. Methods： Using the methods of pathological examination and computer processing,the cardiomyocyte diameters,collagen volume fraction and perivascular circumferential area were observed in patients with myocardial hypertrophy. Angiotensin II（ Ang II） in cardiac local tissue concentration was measured by radioimmunoassay. The protein expression of JAK1,2 and STAT1,3 in myocardial tissue were analyzed using Western blot. Results： The cardiomyocyte diameters,the cardiac collagen volume fraction and perivascular circumferential area of the heart were significantly increased in myocardial hypertrophy group than in control group（ P 〈0. 01,respectively）. The contents of Ang II in cardiac local tissue were also markedly increased in cardiac tissue in myocardial hypertrophy group than in control group（ 179. 3 ± 36. 1）pg / mg tissue vs.（ 103. 2 ± 13. 6） pg / mg tissue,P〈 0. 01）. The protein expression of JAK1,2 and STAT1,3 in myocardial tissue were markedly increased in myocardial hypertrophy group than in control group（ P 〈0. 01,respectively）. Conclusion： This study supports the hypothesis that activation of JAKs-STATs in myocardial hypertrophy may contribute to an involvement of this pathway in the pathogenesis of human cardiac hypertrophy.
出处
《心肺血管病杂志》
2016年第11期864-867,874,共5页
Journal of Cardiovascular and Pulmonary Diseases
