Retinol and estradiol regulation of retinol binding protein and prostaglandin production by porcine uterine epithelial cells in vitro.
Secretion into the uterine lumen follows a precise pattern during early pregnancy. Near the end of the second week of pregnancy and coincident with elongation of conceptuses, retinol, retinol binding protein (RBP), estradiol (E2), and prostaglandins E (PGE) and F (PGF) increase in the uterine lumen, and RBP mRNA increases in the endometrium. In the present studies the potential for E2 (0.1 microM) and retinol (10 microM) to regulate RBP and PG production by cultured luminal (LEC) and glandular (GEC) epithelial cells collected from postpubertal females and LEC from prepubertal gilts was examined. Endometrial tissue was collected surgically from cyclic and pregnant females (n = 8) on d 10 and 13 postestrus (first day of estrus = d 0) and from 120- and 150-d-old prepubertal gilts that were treated with progesterone (P4) (2.2 mg x kg(-1) x d(-1), n = 6) or corn oil (n = 6) for 14 d prior to tissue collection. The LEC from postpubertal females responded to retinol with increased (P < 0.05) RBP, PGE, and PGF in culture medium and increased (P < 0.07) RBP mRNA but E2 decreased (P < 0.05) RBP and RBP mRNA and had no effect on prostaglandins. No E2 or retinol effects on secretions of GEC occurred in vitro, but a day x pregnancy status interaction (P < 0.06) affected PGE output by the GEC. Secretion of PGE was greater when GEC were collected on d 10 of pregnancy than from d-10 cyclic or d-13 pregnant or cyclic females. Both E2 and retinol stimulated (P < 0.05) secretion of RBP by LEC isolated from prepubertal gilts, but their effects were not additive. In vivo treatment of prepubertal gilts with P4 increased (P < 0.05) RBP and decreased (P < 0.05) PG production by LEC in vitro. Therefore responses to E2 and retinol differ between pre- and post-pubertal females, and retinol may function in the regulation of endometrial RBP and PG secretion.
Groothuis
P G
PG
Department of Animal Sciences and Industry, Kansas State University, Manhattan 66506, USA.
McGuire
W J
WJ
Vallett
J L
JL
Grieger
D M
DM
Davis
D L
DL
D000818:Animals; D004717:Endometrium / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology* / Q000502:physiology; D005260:Female; D066298:In Vitro Techniques; D011247:Pregnancy; D011374:Progesterone / Q000097:blood / Q000502:physiology; D011453:Prostaglandins / Q000378:metabolism*; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012177:Retinol-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D013552:Swine / Q000502:physiology*; D013997:Time Factors; D014599:Uterus; D014801:Vitamin A / Q000494:pharmacology* / Q000502:physiology
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D012333:RNA, Messenger; D012177:Retinol-Binding Proteins; D014801:Vitamin A; D011374:Progesterone; D004958:Estradiol