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Progestogens stimulate prostacyclin production by human endothelial cells
C Hermenegildo1, P J Oviedo, M C García-Martínez
1Research Unit, Hospital Clínico Universitario of Valencia and Department of Physiology, Faculty of Medicine and Dentistry, University of Valencia, 46010 Spain. carlos.hermenegildo@uv.es
Human Reproduction (Oxford, England)
|March 1, 2005
Summary
Progesterone and medroxyprogesterone acetate enhance prostacyclin production in endothelial cells by activating progesterone receptors and increasing cyclooxygenase (COX) enzymes. This finding clarifies progestogen effects on vascular health.
Area of Science:
- Endocrinology
- Vascular Biology
- Cell Physiology
Background:
- Progestogen effects on endothelial cells are understudied.
- Prostacyclin, a vasodilator, is synthesized via cyclooxygenase (COX) enzymes.
- This study investigates progesterone and medroxyprogesterone acetate (MPA) impact on prostacyclin.
Purpose of the Study:
- To examine how progesterone and MPA affect prostacyclin production in human umbilical vein endothelial cells (HUVEC).
- To determine the role of progesterone receptors and COX enzymes in mediating these effects.
Main Methods:
- HUVEC were treated with varying concentrations of progesterone or MPA.
- Prostacyclin release, COX expression (mRNA and protein), and receptor involvement were analyzed.
- Selective COX inhibitors and a progesterone receptor antagonist (RU-486) were used.
Main Results:
- Both progestogens dose- and time-dependently increased prostacyclin release.
- Progesterone and MPA elevated both COX-1 and COX-2 mRNA and protein levels.
- Effects were blocked by RU-486, confirming progesterone receptor mediation.
- COX inhibitors reduced basal and progestogen-induced prostacyclin release.
Conclusions:
- Progesterone and MPA stimulate HUVEC prostacyclin production.
- This stimulation is mediated via progesterone receptors.
- Enhanced expression and activity of both COX-1 and COX-2 are key mechanisms.