TY - JOUR
T1 - Regulation of endometrial prostaglandin F2α synthesis during luteolysis and early pregnancy in cattle
AU - Okuda, K.
AU - Miyamoto, Y.
AU - Skarzynski, D. J.
N1 - Funding Information:
Supported by Grants-in-Aid for Scientific Research (B) from the Japan Society for the Promotion of Science (JSPS; 11556054), and from the Polish State Committee for Scientific Research (KBN 5 P06K 003 21).
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2002/7
Y1 - 2002/7
N2 - Luteal regression is caused by a pulsatile release of prostaglandin (PG) F2α from the uterus in the late luteal phase in most mammals including cattle. Although it has been proposed in ruminants that pulsatile PGF2α secretion is generated by a positive feedback loop between luteal and/or hypophyseal oxytocin and uterine PGF2α, the bovine endometrium may possess other mechanisms for initiation of luteolytic PGF2α secretion. It has been recently demonstrated that tumor necrosis factor-α (TNF-α) stimulates PGF2α output from bovine endometrial tissue not only during the follicular phase but also during the late luteal phase, suggesting that TNF-α is a factor in the initiation of luteolysis in cattle. Furthermore, our recent study has shown that IFN-τ suppresses the action of TNF-α on PGF2α synthesis by the bovine endometrium in vitro, suggesting that IFN-τ plays a luteoprotective role by inhibiting TNF-α-induced PGF2α production in early pregnancy. On the other hand, factors other than oxytocin or TNF-α have also been suggested to be involved in the regulation of PGF2α synthesis by bovine endometrium. The purpose of this review is to summarize our current understanding of the endocrine mechanisms that regulate the timing and pattern of uterine PGF2α secretion during the estrous cycle and early pregnancy.
AB - Luteal regression is caused by a pulsatile release of prostaglandin (PG) F2α from the uterus in the late luteal phase in most mammals including cattle. Although it has been proposed in ruminants that pulsatile PGF2α secretion is generated by a positive feedback loop between luteal and/or hypophyseal oxytocin and uterine PGF2α, the bovine endometrium may possess other mechanisms for initiation of luteolytic PGF2α secretion. It has been recently demonstrated that tumor necrosis factor-α (TNF-α) stimulates PGF2α output from bovine endometrial tissue not only during the follicular phase but also during the late luteal phase, suggesting that TNF-α is a factor in the initiation of luteolysis in cattle. Furthermore, our recent study has shown that IFN-τ suppresses the action of TNF-α on PGF2α synthesis by the bovine endometrium in vitro, suggesting that IFN-τ plays a luteoprotective role by inhibiting TNF-α-induced PGF2α production in early pregnancy. On the other hand, factors other than oxytocin or TNF-α have also been suggested to be involved in the regulation of PGF2α synthesis by bovine endometrium. The purpose of this review is to summarize our current understanding of the endocrine mechanisms that regulate the timing and pattern of uterine PGF2α secretion during the estrous cycle and early pregnancy.
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U2 - 10.1016/S0739-7240(02)00161-3
DO - 10.1016/S0739-7240(02)00161-3
M3 - Article
C2 - 12142242
AN - SCOPUS:0036638156
SN - 0739-7240
VL - 23
SP - 255
EP - 264
JO - Domestic Animal Endocrinology
JF - Domestic Animal Endocrinology
IS - 1-2
ER -