蛋白磷酸酶在心肌肥厚发生中的细胞内信号转导作用

：To study the signal transduction mechanisms in myocardial hypertrophy and cardiovascular remodeling, we observed protein phosphatase of its change in hypertrophy and cardiovascular remodeling, its regulation on the nucleus reaction responded to extracellular stimulating signals, and its interaction with protein kinase. We found cardiovascular remodeling in spontaneously hypertensive rats bears on the decrease of mitogen-activated protein kinase phosphatase-1(MKP-1) expression as well as the increased expression of mitogen-activated protein kinase(MAPK). Besides, MKP-1 may play a role in hypertensive cardiovascular remodeling since its effect we observed in the regulation of vascular remodeling with angiotensinⅡ. All this gives a new thoughway for the researchs of cellular molecular mechanism and sighaling transduction pathway in myocardial hypertrophy and cardiovascular remodeling, and for the study of "Ying-Yang" regulation in protein phosphorylation-dephosphorylation.

为阐明心肌肥厚的细胞信号转导机制，本工作从蛋白磷酸化----去磷酸化调节出发，拟研究蛋白磷酸酶（丝裂素活化蛋白激酶特异磷酸酶和钙调神经磷酸酶）在心肌肥厚发病中的变化规律，对肥厚刺激时细胞核反应的调控作用，以及它们与蛋白激酶系统间的相互调节关系，以期提出对心肌肥厚发病的细胞分子机制的新认识。.