title: Prostaglandin E1 (PGE1), but not prostaglandin E2 (PGE2), alters luteal and endometrial luteinizing hormone (LH) occupied and unoccupied LH receptors and mRNA for LH receptors in ovine luteal tissue to prevent luteolysis.
abstract: Loss of luteal progesterone secretion at the end of the ovine estrous cycle is via uterine PGF(2)alpha secretion. However, uterine PGF(2)alpha secretion is not decreased during early pregnancy in ewes. Instead, the embryo imparts a resistance to PGF(2)alpha. Prostaglandins E (PGE; PGE(1)+PGE(2)) are increased in endometrium and uterine venous blood during early pregnancy in ewes to prevent luteolysis. Chronic intrauterine infusion of PGE(1) or PGE(2) prevents spontaneous or IUD, estradiol-17beta, or PGF(2)alpha-induced premature luteolysis in nonbred ewes. The objective was to determine whether chronic intrauterine infusion of PGE(1) or PGE(2) affected mRNA for LH receptors, occupied and unoccupied receptors for LH in luteal and caruncular endometrium, and luteal function. Ewes received Vehicle, PGE(1), or PGE(2) every 4h from days 10 to 16 of the estrous cycle via a cathether installed in the uterine lumen ipsilateral to the luteal-containing ovary. Jugular venous blood was collected daily for analysis of progesterone and uterine venous blood was collected on day-16 for analysis of PGF(2)alpha and PGE. Corpora lutea and caruncular endometrium were collected from day-10 preluteolytic control ewes and day-16 ewes treated with Vehicle, PGE(1) or PGE(2) for analysis of the mRNA for LH receptors and occupied and unoccupied receptors for LH. Luteal weights on day-16 in ewes treated with PGE(1) or PGE(2) and day-10 control ewes were similar (P>or=0.05), but were greater (P<or=0.05) than in day-16 Vehicle-treated ewes. Progesterone profiles on days 10-16 differed (P<or=0.05) among treatment groups: PGE(1)>PGE(2)>Vehicle-treated ewes. Concentrations of PGF(2)alpha and PGE in uterine venous plasma on day-16 were similar (P>or=0.05) in the three treatment groups. Luteal mRNA for LH receptors and unoccupied and occupied LH receptors were similar (P>or=0.05) in day-10 control ewes and day-16 ewes treated with PGE(2) and were lower (P<or=0.05) in day-16 Vehicle-treated ewes. PGE(2) prevented loss (P<or=0.05) of day-16 luteal mRNA for LH receptors and occupied and unoccupied LH receptors. Luteal and caruncular tissue mRNA for LH receptors and occupied and unoccupied LH receptors were greater (P<or=0.05) on day-16 of PGE(1)-treated ewes than any treatment group. mRNA for LH receptors and occupied and unoccupied receptors for LH in caruncules were greater (P<or=0.05) in day-16 Vehicle or PGE(2)-treated ewes than in day-10 control ewes. It is concluded that PGE(1) and PGE(2) share some common mechanisms to prevent luteolysis; however, only PGE(1) increased luteal and endometrial mRNA for LH receptors and occupied and unoccupied LH receptors. PGE(2) prevents a decrease in luteal mRNA for LH receptors and occupied and unoccupied receptors for LH without altering endometrial mRNA for LH receptors or occupied and unoccupied receptors for LH.
authors.affiliation: Dept. of HNFAS, University of Hawaii, 1955 East-West Road, Honolulu, HI 96822, USA.
authors.forename: Y S
authors.initials: YS
authors.lastname: Weems
authors.forename: T M
authors.initials: TM
authors.lastname: Nett
authors.forename: L A
authors.initials: LA
authors.lastname: Rispoli
authors.forename: T L
authors.initials: TL
authors.lastname: Davis
authors.forename: D L
authors.initials: DL
authors.lastname: Johnson
authors.forename: T
authors.initials: T
authors.lastname: Uchima
authors.forename: A
authors.initials: A
authors.lastname: Raney
authors.forename: E
authors.initials: E
authors.lastname: Lennon
authors.forename: J
authors.initials: J
authors.lastname: Pang
authors.forename: T
authors.initials: T
authors.lastname: Harbert
authors.forename: G
authors.initials: G
authors.lastname: Bowers
authors.forename: K
authors.initials: K
authors.lastname: Goto
authors.forename: A
authors.initials: A
authors.lastname: Ong
authors.forename: N
authors.initials: N
authors.lastname: Tsutahara
authors.forename: R D
authors.initials: RD
authors.lastname: Randel
authors.forename: C W
authors.initials: CW
authors.lastname: Weems
mesh_terms: D000527:Alprostadil / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D003338:Corpus Luteum / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D015232:Dinoprostone / Q000008:administration & dosage / Q000494:pharmacology; D004717:Endometrium / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D030762:Estrous Cycle / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D007986:Luteinizing Hormone / Q000378:metabolism*; D003341:Luteolysis / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011974:Receptors, LH / Q000235:genetics* / Q000378:metabolism*; D012756:Sheep; D013997:Time Factors
chemical_list: D012333:RNA, Messenger; D011974:Receptors, LH; D007986:Luteinizing Hormone; D000527:Alprostadil; D015232:Dinoprostone