Why does the fallopian tube fail in ectopic pregnancy? The role of activins, inducible nitric oxide synthase, and MUC1 in ectopic implantation
The pathologic expression of candidate molecules by tubes bearing an ectopic pregnancy does not determine the implantation site, but they may be involved in regulation of the trophoblast.
Bassem Refaat, Ph.D., Hannah Simpson, B.Med.Sci., Elizabeth Britton, B.Med.Sci, Jhulan Biswas, M.D., Michael Wells, M.D., John D. Aplin, Ph.D., William Ledger, D.Phil.
Vol 97, Issue 5, Pages 1115-1123
To investigate the role of activin-βA subunit, activin type II receptors, inducible nitric oxide synthase (iNOS), and MUC1 in the pathogenesis of ectopic pregnancy (EP) and their involvement in the determination of the implantation site.
Academic unit of reproductive and developmental medicine.
Four women at the luteal phase, three pseudopregnant women at the time of hysterectomy for benign disease, and 10 archived cases of EP. We collected 14 Fallopian tubes were collected from four women at the luteal phase and three pseudopregnant women at the time of hysterectomy for benign disease; specimens from implantation site, trophoblast and remote sites from the implantation site were collected from 10 archived cases of EP.
Immunohistochemistry and quantitative reverse-transcriptase polymerase chain reaction (RT-PCR).
Main Outcome Measure(s):
Comparison of the expression of candidate molecules between the different groups.
The expression of activin-βA subunit, activin type II receptors, and iNOS was statistically significantly increased and expression of MUC1 statistically significantly decreased in tubes bearing an EP. There was no statistically significant difference in the expression of the candidate molecules between the implantation and remote sites. Candidate molecules were also expressed in the trophoblast.
The pathological expression of candidate molecules by tubes bearing an EP is not involved in the determination of implantation site. Additionally, candidate molecules may play a role in the regulation of trophoblast cells in vivo during early pregnancy.
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