Renin increases human amnion cell prostaglandin E2 biosynthesis

Lundin-Schiller, S. and Mitchell, M.D. (1991) Renin increases human amnion cell prostaglandin E2 biosynthesis. Journal of Clinical Endocrinology & Metabolism, 73 2: 436-440. doi:10.1210/jcem-73-2-436

Author Lundin-Schiller, S.
Mitchell, M.D.
Title Renin increases human amnion cell prostaglandin E2 biosynthesis
Formatted title
Renin increases human amnion cell prostaglandin E2 biosynthesis
Journal name Journal of Clinical Endocrinology & Metabolism   Check publisher's open access policy
ISSN 0021-972X
Publication date 1991-08
Sub-type Article (original research)
DOI 10.1210/jcem-73-2-436
Volume 73
Issue 2
Start page 436
End page 440
Total pages 5
Place of publication Bethesda, MD, U.S.A.
Publisher Endocrine Society
Language eng
Subject 1103 Clinical Sciences
1114 Paediatrics and Reproductive Medicine
Formatted abstract
Chorionic cells are known to produce several protein hormones; among them is prorenin/renin, whose function is unknown at this time. Amnion is contiguous with chorion and plays a part in the mechanism(s) of parturition through increased prostaglandin (PG) production. The purpose of the present study was to determine whether renin has any action on amnion cell PGE2 biosynthesis. Amnion cells in primary monolayer culture were incubated for 16 h with increasing concentrations of renin. Renin induced a concentration-dependent increase in amnion cell PGE2 production (e.g. in picograms of PGE2 per μg protein/16 h; mean ± SEM; n = 4; control, 3.01 ± 0.15; 0.0001 U/mL renin, 9.66 ± 2.0; 0.001 U/mL renin, 10.36 ± 1.91; 0.01 U/mL renin, 10.3 ± 3.36; 0.1 U/mL renin, 13.82 ± 2.1). Significant stimulation of amnion cell PGE2 by renin is not observed until 2 h of incubation; stimulation continues a further 6 h, with little change in the following 8 h. We tested the possibility that renin's stimulatory effects were due to angiotensin-I (AI) and angiotensin-II (AII) formation by testing the effects of AI and AII directly and that of renin in the presence of saralasin, a potent antagonist of AII action. Saralasin did not inhibit the effect of renin, nor was AI or AII alone (10-10-10-6 M) stimulatory. Thus, we believe that chorionic renin may have a novel role in the regulation of amnion cell PGE2 production that is independent of angiotensin formation.
Keyword Primary Culture
Inactive Renin
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: UQ Centre for Clinical Research Publications
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Created: Thu, 26 Aug 2010, 12:58:58 EST