Prostaglandin E2 both stimulates and inhibits adenyl cyclase on platelets: Comparison of effects on cloned EP4 and EP3 prostaglandin receptor subtypes

Prostaglandins Pub Date : 1996-09-01 DOI:10.1016/S0090-6980(96)00095-0

G.-F. Mao, J.-G. Jin, M. Bastepe, S. Ortiz-Vega, B. Ashby

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引用次数: 20

Abstract

The effects of prostaglandin E₂ (PGE₂) on platelet cyclic AMP formation were examined and compared with effects on cloned prostaglandin receptors. PGE₂ gave a weak stimulation of adenyl cyclase in platelets compared with the PGI₂ analog Iloprost. In the presence of the adenyl cyclase stimulator forskolin, the response to PGE₂ was amplified in a synergistic manner. By contrast, in the presence of Iloprost, PGE₂ inhibited cyclic AMP formation. We postulate that the weak platelet response to PGE₂ is due to co-localization of a PGE₂ receptor that couples to stimulation of adenyl cyclase with the EP3 prostaglandin receptor that binds PGE₂ tightly and inhibits adenyl cyclase. In support of this postulate, we compared the responses obtained with platelets with those of cloned EN (stimulatory) and EP3 (inhibitory) prostaglandin receptor subtypes and show similar dose-response curves for stimulation and inhibition of cyclic AMP formation between platelets and cloned receptors.

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前列腺素E2刺激和抑制血小板腺苷环化酶:对克隆EP4和EP3前列腺素受体亚型的影响比较

研究了前列腺素E2 (PGE2)对血小板环AMP形成的影响，并与对克隆前列腺素受体的影响进行了比较。与PGI2类似物Iloprost相比，PGE2对血小板腺苷环化酶的刺激较弱。在腺苷环化酶刺激剂forskolin的存在下，对PGE2的反应以协同方式被放大。相反，在Iloprost存在下，PGE2抑制环AMP的形成。我们假设血小板对PGE2的弱反应是由于PGE2受体与EP3前列腺素受体的共定位，该受体与腺苷环化酶的刺激偶联，EP3前列腺素受体紧密结合PGE2并抑制腺苷环化酶。为了支持这一假设，我们将血小板与克隆的EN(刺激型)和EP3(抑制性)前列腺素受体亚型的反应进行了比较，发现血小板和克隆受体之间刺激和抑制环AMP形成的剂量-反应曲线相似。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Prostaglandins

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