Prostaglandin E2 as a mediator of fever: the role of prostaglandin E (EP) receptors

10.2741/1458 ◽  
2004 ◽  
Vol 9 (1-3) ◽  
pp. 3046 ◽  
Author(s):  
Takakazu Oka
2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Naoto Muraoka ◽  
Kaori Nara ◽  
Fumiya Tamura ◽  
Hidenori Kojima ◽  
Hiroyuki Yamakawa ◽  
...  

2002 ◽  
Vol 404 (2) ◽  
pp. 302-308 ◽  
Author(s):  
Jun Yu ◽  
Gregory N Prado ◽  
Barbara Schreiber ◽  
Paul Polgar ◽  
Peter Polgar ◽  
...  

2011 ◽  
Vol 30 (3-4) ◽  
pp. 465-480 ◽  
Author(s):  
J. E. Rundhaug ◽  
M. S. Simper ◽  
I. Surh ◽  
S. M. Fischer

Endocrines ◽  
2020 ◽  
Vol 1 (1) ◽  
pp. 22-34
Author(s):  
Yao Ye ◽  
Peng Lin ◽  
Junyan Zhu ◽  
Udo Jeschke ◽  
Viktoria von Schönfeldt

Among prostaglandins, Prostaglandin E2 (PGE2) (PGE2) is considered especially important for decidualization, ovulation, implantation and pregnancy. Four major PGE2 receptor subtypes, EP1, EP2, EP3, EP4, as well as peroxisome proliferator-activated receptors (PPARs), mediate various PGE2 effects via their coupling to distinct signaling pathways. This review summarizes up-to-date literatures on the role of prostaglandin E2 receptors in female reproduction, which could provide a broad perspective to guide further research in this field. PGE2 plays an indispensable role in decidualization, ovulation, implantation and pregnancy. However, the precise mechanism of Prostaglandin E2 (EP) receptors in the female reproductive system is still limited. More investigations should be performed on the mechanism of EP receptors in the pathological states, and the possibility of EP agonists or antagonists clinically used in improving reproductive disorders.


2013 ◽  
Vol 33 (4) ◽  
pp. 479-482 ◽  
Author(s):  
Fabrice Dabertrand ◽  
Rachael M Hannah ◽  
Jessica M Pearson ◽  
David C Hill-Eubanks ◽  
Joseph E Brayden ◽  
...  

It has been proposed that prostaglandin E2 (PGE2) is released from astrocytic endfeet to dilate parenchymal arterioles through activation of prostanoid (EP4) receptors during neurovascular coupling. However, the direct effects of PGE2 on isolated parenchymal arterioles have not been tested. Here, we examined the effects of PGE2 on the diameter of isolated pressurized parenchymal arterioles from rat and mouse brain. Contrary to the prevailing assumption, we found that PGE2 (0.1, 1, and 5 μmol/L) constricted rather than dilated parenchymal arterioles. Vasoconstriction to PGE2 was prevented by inhibitors of EP1 receptors. These results strongly argue against a direct role of PGE2 on arterioles during neurovascular coupling.


1975 ◽  
Vol 65 (1) ◽  
pp. 55-63 ◽  
Author(s):  
A. SPÄT ◽  
SARA JÓZAN

SUMMARY Prostaglandin E2 increased aldosterone output by superfused capsular adrenal glands obtained from sodium-repleted, hypophysectomized rats but corticosterone did not show a statistically significant increase. Prostaglandin A2 increased corticosterone but not aldosterone production by incubated capsular glands obtained from sodium-repleted, hypophysectomized rats. Both aldosterone and corticosterone production rates were increased by PGA2 after previous sodium restriction. Corticosterone production rate of the decapsulated adrenal gland was not significantly modified by prostaglandin A2 in a concentration effective on the capsular adrenal gland. A possible role of prostaglandins in the regulation of aldosterone secretion is discussed.


Endocrinology ◽  
2014 ◽  
Vol 155 (4) ◽  
pp. 1466-1475 ◽  
Author(s):  
Soon Ok Kim ◽  
Siabhon M. Harris ◽  
Diane M. Duffy

Prostaglandin E2 (PGE2) is a key mediator of ovulation. All 4 PGE2 receptors (EP receptors) are expressed in the primate follicle, but the specific role of each EP receptor in ovulatory events is poorly understood. To examine the ovulatory events mediated via these EP receptors, preovulatory monkey follicles were injected with vehicle, the PG synthesis inhibitor indomethacin, or indomethacin plus PGE2. An ovulatory dose of human chorionic gonadotropin was administered; the injected ovary was collected 48 hours later and serially sectioned. Vehicle-injected follicles showed normal ovulatory events, including follicle rupture, absence of an oocyte, and thickening of the granulosa cell layer. Indomethacin-injected follicles did not rupture and contained oocytes surrounded by unexpanded cumulus; granulosa cell hypertrophy did not occur. Follicles injected with indomethacin plus PGE2 were similar to vehicle-injected ovaries, indicating that PGE2 restored the ovulatory changes inhibited by indomethacin. Additional follicles were injected with indomethacin plus an agonist for each EP receptor. EP1, EP2, and EP4 agonists each promoted aspects of follicle rupture, but no single EP agonist recapitulated normal follicle rupture as seen in follicles injected with either vehicle or indomethacin plus PGE2. Although EP4 agonist-injected follicles contained oocytes in unexpanded cumulus, the absence of oocytes in EP1 agonist- and EP2 agonist-injected follicles suggests that these EP receptors promote cumulus expansion. Surprisingly, the EP3 agonist did not stimulate any of these ovulatory changes, despite the high level of EP3 receptor expression in the monkey follicle. Therefore, agonists and antagonists selective for EP1 and EP2 receptors hold the most promise for control of ovulatory events in women.


Sign in / Sign up

Export Citation Format

Share Document