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. 2024 Nov;5(4):379-385.
doi: 10.1016/j.xfss.2024.07.007. Epub 2024 Jul 20.

Prostaglandin E2 regulates the plasminogen activator pathway in human endometrial endothelial cells: a new in vitro model to investigate heavy menstrual bleeding

Seifeldin Sadek  1 , Terry A Jacot  2 , Diane M Duffy  3 , David F Archer  4
Affiliations

Prostaglandin E2 regulates the plasminogen activator pathway in human endometrial endothelial cells: a new in vitro model to investigate heavy menstrual bleeding

Seifeldin Sadek et al. F S Sci. 2024 Nov.

Abstract

Objective: To study the role of PGE2 in regulating plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) in human primary endometrial endothelial cells (HEECs) from women with normal menstrual bleeding (NMB) and heavy menstrual bleeding (HMB).

Design: In vitro study using endometrial endothelial cells.

Setting: Research laboratory setting.

Patients: Women with NMB and HMB provided endometrial biopsy samples.

Interventions: Prostaglandin E2 and PGE2 receptor-selective agonists were administered to cultured HEECs.

Main outcome measures: Levels of PAI-1 and tPA in NMB-HEECs and HMB-HEECs after treatment with PGE2 and receptor-selective agonists.

Results: Prostaglandin E2 increased total PAI-1 levels in NMB-HEECs, but not in HMB-HEECs, which had higher baseline PAI-1 levels. PGE2 receptors (PTGER)1 and PTGER2 agonists increased PAI-1 in NMB-HEECs, whereas PTGER3 and PTGER4 did not. Prostaglandin E2 had no effect on tPA levels in either NMB-HEECs or HMB-HEECs.

Conclusions: Prostaglandin E2, through PTGER1 and PTGER2, regulates the plasminogen activator system in NMB-HEECs, suggesting a role in reducing fibrinolytic activity during normal menstrual cycles. The lack of PGE2 effect and elevated baseline PAI-1 in HMB-HEECs support using this in vitro model to further understand prostaglandin pathways in NMB and HMB.

Keywords: Endometrium; endothelial cell; menstrual bleeding; plasminogen activator system; prostaglandin E(2).

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Conflict of interest statement

Declaration of Interests S.S. and T.A.J. report funding from Jones Family Foundation, Eastern Virginia Medical School and Commonwealth Health Research Board for the submitted work. D.M.D. reports funding from Jones Family Foundation, Eastern Virginia Medical School and Commonwealth Health Research Board for the submitted work; funding from NIH, Organon & Co. (product donation – no direct financial support), Wisconsin National Primate Research Center, and American Heart Association; consulting fees from InnovaGyn Inc; InnovaGyn Inc, Chief Science Officer member of the Board of Directors; Society for the Study of Reproduction, Chair, Development Committee unpaid; Federation of American Societies for Experimental Biology (FASEB) Chair, Meetings Committee unpaid; and stock options from InnovaGyn Inc. outside the submitted work. D.F.A. reports funding from Jones Family Foundation, Eastern Virginia Medical School and Commonwealth Health Research Board for the submitted work; grant support for research from Jones Family Foundation at Eastern Virginia Medical School; and stock options as CEO of InnovaGyn, Inc outside the submitted work.

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