Endothelin induction of inositol phospholipid hydrolysis, sarcomere assembly, and cardiac gene expression in ventricular myocytes. A paracrine mechanism for myocardial cell hypertrophy.

Endothelin induction of inositol phospholipid hydrolysis, sarcomere assembly, and cardiac gene expression in ventricular myocytes. A paracrine mechanism for myocardial cell hypertrophy.
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发表时间:
1990-11
期刊:
The Journal of biological chemistry
影响因子:
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通讯作者:
H. Shubeita;Patrick M. McDonough;A. N. Harris;Kirk U. Knowlton;C. C. Glembotski-C.;Joan Heller Brown;Kenneth R. Chien
H. Shubeita;Patrick M. McDonough;A. N. Harris;Kirk U. Knowlton;C. C. Glembotski-C.;Joan Heller Brown;Kenneth R. Chien
中科院分区:
其他
文献类型:
--
作者:
H. Shubeita;Patrick M. McDonough;A. N. Harris;Kirk U. Knowlton;C. C. Glembotski-C.;Joan Heller Brown;Kenneth R. Chien

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本研究探讨了内皮素-1对磷酸肌醇水解,甘油二酯的形成,并利用一个良好的特点培养的新生大鼠心肌细胞模型诱导心肌细胞肥大的影响。在该系统中,肥大反应可以通过心肌细胞大小的增加、单个收缩蛋白(肌球蛋白轻链-2)组装成有组织的收缩单位的增加、收缩蛋白的积累、立即早期基因表达程序的激活和编码收缩蛋白和胚胎蛋白的基因的诱导来评估(Iwaki,K.,Sukhatme,V.,Shubeita,H.E.,Chien,K.R.,(1990)J.Biol.Chem.265,13809-13817)。利用这些标准,本研究的文件,与内皮素-1的刺激可以产生心肌细胞肥大,诱导心钠素在心室细胞的表达和释放,并可以激活心脏特异性基因的转录。此外,内皮素-1刺激磷酸肌醇水解和甘油二酯的积累。它提出,内皮素-1刺激可能代表了一个重要的旁分泌机制,在体内调节心脏的生长和肥大。
The present study examined the effects of endothelin-1 on phosphoinositide hydrolysis, diacylglycerol formation, and the induction of myocardial cell hypertrophy utilizing a well characterized cultured neonatal rat myocardial cell model. In this system, a hypertrophic response can be assessed by increases in myocardial cell size, an increase in the assembly of an individual contractile protein (myosin light chain-2) into organized contractile units, accumulation of contractile proteins, the activation of a program of immediate early gene expression, and the induction of genes encoding contractile and embryonic proteins (Iwaki, K., Sukhatme, V., Shubeita, H.E., Chien, K.R., (1990) J. Biol. Chem. 265, 13809-13817). Utilizing these criteria, the present study documents that stimulation with endothelin-1 can produce myocardial cell hypertrophy, induce the expression and release of ANF in ventricular cells, and can activate the transcription of cardiac-specific genes. In addition, endothelin-1 stimulates phosphoinositide hydrolysis and the accumulation of diacylglycerol. It is proposed that endothelin-1 stimulation may represent an important paracrine mechanism for the in vivo regulation of cardiac growth and hypertrophy.