Nitric oxide (NO) inhibits prostaglandin E2 9-ketoreductase (9-KPR) activity in human fetal membranes
| Autor: | María Laura Ribeiro, S. Billi, E. Lombardi, G. Di Girolamo, Ana Maria Franchi, Micaela S. Sordelli, Mariana Farina |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
medicine.medical_specialty
Tocolytic agent Physiology Metabolite medicine.medical_treatment Extraembryonic Membranes Dinoprost Nitric Oxide Biochemistry Dinoprostone Nitric oxide Contractility chemistry.chemical_compound Pregnancy Internal medicine medicine Humans Nitric Oxide Donors Pharmacology Fetus Dose-Response Relationship Drug biology Myometrium Cell Biology Middle Aged Nitric oxide synthase Endocrinology Gene Expression Regulation chemistry Prostaglandin-Endoperoxide Synthases Hydroxyprostaglandin Dehydrogenases biology.protein Female lipids (amino acids peptides and proteins) Nitric Oxide Synthase Prostaglandin E |
| Zdroj: | Prostaglandins & Other Lipid Mediators. 79:260-270 |
| ISSN: | 1098-8823 |
| DOI: | 10.1016/j.prostaglandins.2006.02.004 |
| Popis: | Nitric oxide (NO) synthesized by fetal membranes may act either directly inhibiting myometrium contractility or indirectly interacting with tocolytic agents as prostaglandins (PGs). Here we examined if NO could modulate prostaglandin E(2) 9-ketoreductase (9-KPR) activity in human fetal membranes (HFM). 9-KPR is the enzyme that converts PGE(2) into PGF(2alpha), the main PGs known to induce uterine contractility at term. Chorioamnion explants obtained from elective caesareans were incubated with aminoguanidine (AG), an iNOS inhibitor, or NOC-18, a NO donor. NOC-18 (2mM) increased PGE(2) production and diminished PGF(2alpha) synthesis in HFM. AG presented the opposite effect. When we evaluated the activity of 9-KPR by the conversion of [(3)H]-PGE(2) into [(3)H]-PGF(2alpha) and 13,14-dihidro-15-keto prostaglandin F(2alpha) (the PGF(2alpha) metabolite), we found that NOC-18 inhibited 9-KPR activity. Interestingly, AG did not elicit any effect on 9-KPR but l-NAME, a non-selective NOS inhibitor, significantly increased its activity. Our data suggests that exogenous NO inhibits 9-KPR activity in HFM, thus modulating the synthesis of important labor mediators as PGF(2alpha). |
| Databáze: | OpenAIRE |
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