{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T07:11:27Z","timestamp":1792048287627,"version":"4.4.0"},"reference-count":0,"publisher":"Bioscientifica","issue":"3","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:p>\n                    In luteinizing granulosa cells, prostaglandin E\n                    <jats:sub>2<\/jats:sub>\n                    (PGE\n                    <jats:sub>2<\/jats:sub>\n                    ) can exert luteotrophic actions, apparently via the cAMP signalling pathway. In addition to stimulating progesterone synthesis, PGE\n                    <jats:sub>2<\/jats:sub>\n                    can also stimulate oxidation of the physiological glucocorticoid, cortisol, to its inactive metabolite, cortisone, by the type 1 11\u03b2-hydroxysteroid dehydrogenase (11\u03b2HSD1) enzyme in human granulosa\u2013lutein cells. Having previously shown these human ovarian cells to express functional G-protein coupled, E-series prostaglandin (PTGER)1, PTGER2 and PTGER4 receptors, the aim of this study was to delineate the roles of PTGER1 and PTGER2 receptors in mediating the effects of PGE\n                    <jats:sub>2<\/jats:sub>\n                    on steroidogenesis and cortisol metabolism in human granulosa\u2013lutein cells. PGE\n                    <jats:sub>2<\/jats:sub>\n                    -stimulated concentration-dependent increases in both progesterone production and cAMP accumulation (by 1.9 \u00b1 0.1- and 18.7 \u00b1 6.8-fold respectively at 3000 nM PGE\n                    <jats:sub>2<\/jats:sub>\n                    ). While a selective PTGER1 antagonist, SC19220, could partially inhibit the steroidogenic response to PGE\n                    <jats:sub>2<\/jats:sub>\n                    (by 55.9 \u00b1 4.1% at 1000 nM PGE\n                    <jats:sub>2<\/jats:sub>\n                    ), co-treatment with AH6809, a mixed PTGER1\/PTGER2 receptor antagonist, completely abolished the stimulation of progesterone synthesis at all tested concentrations of PGE\n                    <jats:sub>2<\/jats:sub>\n                    and suppressed the stimulation of cAMP accumulation. Both PGE\n                    <jats:sub>2<\/jats:sub>\n                    and butaprost (a preferential PTGER2 receptor agonist) stimulated concentration-dependent increases in cortisol oxidation by 11\u03b2HSD1 (by 42.5 \u00b1 3.1 and 40.0 \u00b1 3.0% respectively, at PGE\n                    <jats:sub>2<\/jats:sub>\n                    and butaprost concentrations of 1000 nM). Co-treatment with SC19220 enhanced the ability of both PGE\n                    <jats:sub>2<\/jats:sub>\n                    and butaprost to stimulate 11\u03b2HSD1 activity (by 30.2 \u00b1 0.2 and 30.5 \u00b1 0.6% respectively), whereas co-treatment with AH6809 completely abolished the 11\u03b2HSD1 responses to PGE\n                    <jats:sub>2<\/jats:sub>\n                    and butaprost. These findings implicate the PTGER2 receptor\u2013cAMP signalling pathway in the stimulation of progesterone production and 11\u03b2HSD1 activity by PGE\n                    <jats:sub>2<\/jats:sub>\n                    in human granulosa\u2013lutein cells.\n                  <\/jats:p>","DOI":"10.1677\/joe-07-0128","type":"journal-article","created":{"date-parts":[[2007,8,30]],"date-time":"2007-08-30T15:18:42Z","timestamp":1188487122000},"page":"595-602","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":21,"title":["PTGER1 and PTGER2 receptors mediate regulation of progesterone synthesis and type 1 11\u03b2-hydroxysteroid dehydrogenase activity by prostaglandin E2 in human granulosa\u2013lutein cells"],"prefix":"10.1530","volume":"194","author":[{"given":"C","family":"Chandras","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T E","family":"Harris","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A Lo\u0301pez","family":"Bernal","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D R E","family":"Abayasekara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A E","family":"Michael","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Journal of Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/joe.bioscientifica.com\/view\/journals\/joe\/194\/3\/1940595.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/joe.bioscientifica.com\/downloadpdf\/journals\/joe\/194\/3\/1940595.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:53:00Z","timestamp":1784555580000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/joe\/article\/194\/3\/595-602\/21438"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2007,9]]},"references-count":0,"journal-issue":{"issue":"3"},"URL":"https:\/\/doi.org\/10.1677\/joe-07-0128","relation":{},"ISSN":["0022-0795","1479-6805"],"issn-type":[{"value":"0022-0795","type":"print"},{"value":"1479-6805","type":"electronic"}],"subject":[],"published":{"date-parts":[[2007,9]]}}}