Comparison of the effects of GnRH-I and GnRH-II on HCG synthesis and secretion by first trimester trophoblast

Citation
D. Islami et al., Comparison of the effects of GnRH-I and GnRH-II on HCG synthesis and secretion by first trimester trophoblast, MOL HUM REP, 7(1), 2001, pp. 3-9
Citations number
49
Categorie Soggetti
Cell & Developmental Biology
Journal title
MOLECULAR HUMAN REPRODUCTION
ISSN journal
13609947 → ACNP
Volume
7
Issue
1
Year of publication
2001
Pages
3 - 9
Database
ISI
SICI code
1360-9947(200101)7:1<3:COTEOG>2.0.ZU;2-W
Abstract
Gonadotrophin-releasing hormone (GnRH) is an important factor in the regula tion of the synthesis and secretion of gonadotrophins from the pituitary gl and, An isoform of this decapeptide, GnRH-II, with an amino acid sequence 7 0% homologous to GnRH-I, has been recently described. Since the physiologic al effects of GnRH-II are not yet known, we undertook the present study to see whether GnRH-II could be involved in the secretion and synthesis of HCG in first trimester trophoblast. We incubated cytotrophoblastic cells (CTB) with GnRH-I or GnRH-II, for 4 or 96 h and collected the media at different times thereafter. We also performed experiments with placental tissue, whe re GnRH-I or GnRH-II was added to perifused placental explants, and samples were collected every 3 min. Total amounts of human chorionic gonadotrophin (HCG) were measured in all samples by enzyme-linked immunosorbent assay. G nRH-I was more potent than GnRH-II when incubated for 4 h with CTB, as indi cated by increased HCG secretion at 8 h and at 24 h. GnRH-I, but not GnRH-I I, down-regulated HCG secretion when incubated for 96 h, GnRH-I significant ly increased HCG secretion by the explants, while GnRH-II had a lesser effe ct. Both induced a pulse of HCG immediately after their injection. Our data show that GnRH-I has more effect than GnRH-II on HCG synthesis and secreti on. This difference could be explained by different pathways of GnRH degrad ation, different receptor affinities, or even by different types of placent al GnRH receptor.