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

{"title":"Prostaglandin E2 both stimulates and inhibits adenyl cyclase on platelets: Comparison of effects on cloned EP4 and EP3 prostaglandin receptor subtypes","authors":"G.-F. Mao, J.-G. Jin, M. Bastepe, S. Ortiz-Vega, B. Ashby","doi":"10.1016/S0090-6980(96)00095-0","DOIUrl":null,"url":null,"abstract":"<div>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.</div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00095-0","citationCount":"20","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0090698096000950","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

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.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

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。

求助全文

约1分钟内获得全文去求助

来源期刊

Prostaglandins

自引率

0.00%

发文量

期刊最新文献

Editorial The Isoprostanes: A Perspective Nomenclature of Isoprostanes: A Proposal Occurrence of 13(S)-Hydroxyoctadecadienoic Acid in Biological Samples Urinary Thromboxane B2 in Cardiac Transplant Patients as a Screening Method of Rejection