Elevated expression of catechol-O-methyltransferase is associated with labor and increased prostaglandin E2 production by human fetal membranes
- Hassan Harirah,
- Chandrasekhar Thota,
- Melissa J. Wentz,
- Wahiduz Zaman,
- Ayman Al-Hendy(corresponding author)
- University of Texas Medical Branch at Galveston,
- Meharry Medical College,
- Texas Nerve and Paralysis Institute
Abstract
Objective: The purpose of this study was to evaluate the expression and function of catechol-O-methyltransferase in human fetal membranes at term. Study Design: Fetal membranes obtained from women between 38-42 weeks of gestation, after (1) vaginal delivery with spontaneous labor and (2) prelabor elective cesarean section (no labor), were assayed for catechol-O-methyltransferase expression using quantitative real-time polymerase chain reaction analysis, immunohistochemistry, and Western blot analysis. Prostaglandin E2 secretion from amnion and choriodecidua explants treated with or without catechol-O-methyltransferase inhibitor was assayed by enzyme-linked immunosorbent analysis. Results: Amnion layer of fetal membranes from laboring women expressed significantly higher levels of catechol-O-methyltransferase, compared with those from women with no labor. Catechol-O-methyltransferase was higher in the amnion layer than in choriodecidua. Selective catechol-O-methyltransferase inhibition significantly decreased prostaglandin E2 production from fetal membranes. Conclusion: Labor increases catechol-O-methyltransferase expression in the amnion of human fetal membranes. Selective catechol-O-methyltransferase inhibition decreased prostaglandin E2 secretion in fetal explant cultures, suggesting a role for catechol-O-methyltransferase in human labor and delivery.
Publication Information
Output type
Original language
English (US)Pages from-to (Number of pages)
Pages 496.e1-496.e7Journal (Volume, Issue Number)
American journal of obstetrics and gynecology (Volume 201, Issue 5)Publication milestones
- Published - 11/2009
Publication status
ISSN
0002-9378Publication IDs
- Scopus: 70350575756
- PubMed: 19664748
