Ovine prostaglandin F-2 alpha receptor - Steroid influence on steady-statelevels of luteal mRNA

Citation
Pb. Hoyer et al., Ovine prostaglandin F-2 alpha receptor - Steroid influence on steady-statelevels of luteal mRNA, ENDOCRINE, 10(2), 1999, pp. 105-111
Citations number
36
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
ENDOCRINE
ISSN journal
1355008X → ACNP
Volume
10
Issue
2
Year of publication
1999
Pages
105 - 111
Database
ISI
SICI code
1355-008X(199904)10:2<105:OPFAR->2.0.ZU;2-P
Abstract
Expression of the receptor for prostaglandin F-2 alpha (PGF(2 alpha)) is de creased in the ovine corpus luteum during regression and increased in early pregnancy. This study was designed to evaluate the influence of progestero ne and/or 17 beta-estradiol (E-2) on this regulation. Circulating progester one (functional regression) and luteal PGF receptor mRNA decreased (p < 0.0 5) within 8 h of PGF(2 alpha)-induced luteal regression in midluteal phase (day 10; d 10) ewes; however, internucleosomal DNA fragmentation (structura l regression) was not yet increased. Additionally, luteal PGF receptor mRNA and circulating progesterone were greater (p < 0.05) in pregnant than in n onpregnant ewes on d 14, but not on d 12, Twelve hours following injection of d 10 ewes with E-2, steady-state levels of mRNA for PGF receptor were de creased (p < 0.05), although circulating progesterone and DNA laddering wer e unchanged. Conversely, luteal mRNA for PGF receptor was increased (p < 0. 05) by E-2 treatment in hysterectomized ewes, These results provide evidenc e that (1) luteal PGF receptor expression parallels circulating progesteron e levels during functional regression and in early pregnancy, but (2) expre ssion of PGF receptor can be dissociated from alterations in circulating pr ogesterone by injection with E-2. Additionally, decreased PGF receptor expr ession initiated by E-2 is uterine-dependent, whereas the direct luteal eff ect (hysterectomized ewes) of E-2 is a stimulation of PGF receptor expressi on. These results collectively support the belief that the apparent downreg ulation of PGF receptor during luteal regression is associated with uterine -derived PGF(2 alpha) and its intracellular effects rather than with altera tions in ovarian steroid production.