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内皮素在无血清培养基中刺激新生大鼠心肌细胞肥大和收缩。

Endothelin stimulates hypertrophy and contractility of neonatal rat cardiac myocytes in a serum-free medium.

作者信息

Suzuki T, Hoshi H, Mitsui Y

机构信息

Bio-Science Laboratory, Inc., Yamagata, Japan.

出版信息

FEBS Lett. 1990 Jul 30;268(1):149-51. doi: 10.1016/0014-5793(90)80995-u.

Abstract

The effect of endothelin (ET) on rat cardiac myocytes cultured in a serum-free, defined medium was determined. ET simulated cardiac myocyte hypertrophy in a dose-dependent manner as determined by the protein synthesis and cell surface area. Since the myocyte hypertrophy was abolished by H-7, a protein kinase C inhibitor, ET-receptor mediated protein kinase C activation may be involved in cardiac myocyte hypertrophy. At the same time, ET also stimulated myocyte contractility in this medium, and this stimulatory effect was inhibited by nicardipine. This result indicates that the influx of extracellular calcium ion is necessary for the stimulation of contractility induced by ET.

摘要

研究了内皮素(ET)对在无血清、特定培养基中培养的大鼠心肌细胞的作用。通过蛋白质合成和细胞表面积测定,ET以剂量依赖方式模拟心肌细胞肥大。由于蛋白激酶C抑制剂H-7可消除心肌细胞肥大,因此ET受体介导的蛋白激酶C激活可能参与心肌细胞肥大。同时,ET也刺激了该培养基中的心肌细胞收缩性,且这种刺激作用被尼卡地平抑制。该结果表明细胞外钙离子内流对于ET诱导的收缩性刺激是必需的。

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