Proto-oncogene fos (c-fos) expression in the heart.
Proto-oncogene fos (c-fos) expression in the heart.
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发表时间：
1987
期刊：
影响因子：
8
通讯作者：
T. Barka;H. vanderNoen;Shaw Pa
中科院分区：
文献类型：
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作者：
T. Barka;H. vanderNoen;Shaw Pa
给予 β-肾上腺素能激动剂异丙肾上腺素可导致小鼠、大鼠和叙利亚仓鼠心脏中 c-fos mRNA 的稳态水平显着快速增加。异丙肾上腺素对 c-fos 表达的刺激被 β-肾上腺素能拮抗剂普萘洛尔抑制。异丙肾上腺素激活 c-fos 基因可能不需要通过电压依赖性钙通道增加 Ca2+ 流入，因为钙通道阻滞剂维拉帕米、硝苯地平和地尔硫卓对药物诱导 c-fos 没有影响。在大鼠心脏中，α-肾上腺素能激动剂去氧肾上腺素、组胺和前列腺素 E1 也刺激 c-fos 表达。组胺诱导的 c-fos 基因表达被组胺 H1 受体拮抗剂吡拉明阻断，但不能被 H2 受体拮抗剂雷尼替丁和西咪替丁阻断。结论是，在心脏中，增加 cAMP 和胞质 Ca2+ 的激素（例如 β-肾上腺素激动剂和前列腺素 E1）和/或刺激肌醇磷脂周转的激素（例如 α-肾上腺素激动剂和组胺 H1-受体激动剂）调节 c-fos 基因表达。 fos蛋白可能在调节心脏功能以及心脏肥大、变性和坏死的神经递质和激素机制中发挥作用。
Administration of the beta-adrenergic agonist isoproterenol led to a marked rapid increase in the steady-state level of c-fos mRNA in the heart of mice, rats, and Syrian hamsters. Stimulation of c-fos expression by isoproterenol was inhibited by the beta-adrenergic antagonist propranolol. An increase in Ca2+ influx through voltage-dependent calcium channels is probably not required for the activation of the c-fos gene by isoproterenol since the calcium channel blockers verapamil, nifedipine, and diltiazem had no effect on the induction of c-fos by the drug. In the heart of the rat, c-fos expression was also stimulated by the alpha-adrenergic agonist phenylephrine, histamine, and prostaglandin E1. The histamine-induced expression of the c-fos gene was blocked by the histamine H1-receptor antagonist pyrilamine but not by H2-receptor antagonists ranitidine and cimetidine. It is concluded that in the heart, hormones which increase cAMP and cytosolic Ca2+, such as beta-adrenergic agonists and prostaglandin E1, and/or stimulate the turnover of inositol phospholipids, such as alpha-adrenergic agonists and histamine H1-receptor agonists, regulate c-fos gene expression. The fos protein is likely to play a role in the mechanisms of neurotransmitters and hormones that modulate the functioning of the heart and of cardiac hypertrophy, degeneration and necrosis.