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首页> 外文会议>International Symposium on Regulation of Enzyme Activity and Synthesis in Normal and Neoplastic Tissues >gration of protein kinase signaling pathwaysin cardiac myocytes: signaling to and from theextracellular signal-regulated kinases
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gration of protein kinase signaling pathwaysin cardiac myocytes: signaling to and from theextracellular signal-regulated kinases

机译：蛋白质激酶信号传导途径心脏肌细胞的腺体：向外信号调节激酶的信号传导

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Cardiac myocytes (the contractile cells of the heart) are terminally differentiatedcells which withdraw from the cell cycle in the perinatal period. Subsequent growthof the heart reflects an increase in size of pre-existing cardiac myocytes. In responseto pathological stimuli, these cells can undergo further growth to accommodate anincreased work-load resulting from, for example, hypertension, or to compensate forcells which may be lost as a result of myocardial infarction. This hypertrophicgrowth response of the cardiac myocytes is associated with morphological changesincluding an increase in cell size and myofibrillar content, in addition to changes ingene and protein expression (Sugden and Clerk, 1998). The underlying mechanismsassociated with cardiac myocyte hypertrophy have been under intense investigationusing either primary cultures of neonatal cardiac myocytes or freshly isolated adultmyocytes (from rat or mouse). It is probable that the myocytes respond to a numberof locally released neurohumoral factors [e.g. endothelin-1 (ET-1); norepinephrineacting through the oc-adrenergic receptor] which activate a variety of intracellularsignaling pathways (Sugden, 2001, 2003). ET-1 and the synthetic a-adrenergicagonist phenylephrine (PE) stimulate cardiac myocyte hypertrophy in vitro, actingthrough their respective heterotrimeric G protein-coupled receptors (GPCRs)(Sugden, 2001, 2003). Both ET-1 and PE stimulate Gaq to activate phospholipaseCfl (Sugden and Clerk, 1997). In cardiac myocytes, as in other cells, the subsequenthydrolysis of phosphatidylinositol 4,5 bisphosphate [PtdIns(4,5)P2] produces inositol1,4,5 trisphosphate (InsP3), the formation of which at early time points can be usedas an index of phospholipase Cfl activity (Clerk and Sugden, 1997b).
机译：心肌细胞（心脏的收缩细胞）是终点分化，其在围产期中从细胞周期中退出。随后心脏的生长反映了预先存在的心肌细胞的大小增加。在响应病理刺激中，这些细胞可以进一步增长以适应由例如高血压的致压力的工纳，或者补偿可能由于心肌梗死而可能丢失的压织。外，心肌细胞的这种肥大生长响应与形态学的变化包括细胞尺寸和肌原纤维含量的增加，除了改变Ingene和蛋白表达（Sugden and Clerk，1998）。用心肌细胞肥大的潜在机制已经强烈调查新生儿心肌细胞或新生儿孤立的成人细胞（来自大鼠或小鼠）的原发性培养物。肌细胞可能响应局部释放的神经胃部因子的Numberof [例如内皮素-1（ET-1）;通过OC-adrenergic受体进行去甲肾上腺素，其激活各种细胞内血管途径（Sugden，2001,2003）。 ET-1和合成的A-肾上腺蛋白剂苯妥ET-1和PE刺激Gaq激活磷脂磷纤维（Sugden and Clerk，1997）。在心脏肌细胞中，如在其他细胞中，磷脂酰肌醇4,5-双磷酸盐[PTDINS（4,5）P2]的后氢化产生肌醇1,4,5三磷酸（Insp3），在早期点的形成可以使用指数磷脂酶CFL活性（职员和ugden，1997b）。

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