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Physiological Reviews, Vol. 79, No. 2, April 1999, pp. 263-323
Copyright ©1999 by the American Physiological Society
Worcester Foundation for Biomedical Research, Shrewsbury, Massachusetts
McCracken, John A.,
Edward E. Custer, and
Justin C. Lamsa.
In many nonprimate mammalian species,
cyclical regression of the corpus luteum (luteolysis) is caused by the
episodic pulsatile secretion of uterine PGF2
, which acts
either locally on the corpus luteum by a countercurrent mechanism or,
in some species, via the systemic circulation. Hysterectomy in these
nonprimate species causes maintenance of the corpora lutea, whereas in
primates, removal of the uterus does not influence the cyclical
regression of the corpus luteum. In several nonprimate species, the
episodic pattern of uterine PGF2
secretion appears to be
controlled indirectly by the ovarian steroid hormones estradiol-17
and progesterone. It is proposed that, toward the end of the luteal
phase, loss of progesterone action occurs both centrally in the
hypothalamus and in the uterus due to the catalytic reduction
(downregulation) of progesterone receptors by progesterone. Loss of
progesterone action may permit the return of estrogen action, both
centrally in the hypothalamus and peripherally in the uterus. Return of central estrogen action appears to cause the hypothalamic oxytocin pulse generator to alter its frequency and produce a series of intermittent episodes of oxytocin secretion. In the uterus, returning estrogen action concomitantly upregulates endometrial oxytocin receptors. The interaction of neurohypophysial oxytocin with oxytocin receptors in the endometrium evokes the secretion of luteolytic pulses
of uterine PGF2
. Thus the uterus can be regarded as a
transducer that converts intermittent neural signals from the hypothalamus, in the form of episodic oxytocin secretion, into luteolytic pulses of uterine PGF2
. In ruminants,
portions of a finite store of luteal oxytocin are released
synchronously by uterine PGF2
pulses. Luteal oxytocin in
ruminants may thus serve to amplify neural oxytocin signals that are
transduced by the uterus into pulses of PGF2
. Whether
such amplification of episodic PGF2
pulses by luteal
oxytocin is a necessary requirement for luteolysis in ruminants remains
to be determined. Recently, oxytocin has been reported to be produced
by the endometrium and myometrium of the sow, mare, and rat. It is
possible that uterine production of oxytocin may act as a supplemental
source of oxytocin during luteolysis in these species. In primates,
oxytocin and its receptor and PGF2
and its receptor have
been identified in the corpus luteum and/or ovary. Therefore, it is
possible that oxytocin signals of ovarian and/or neural origin may be
transduced locally at the ovarian level, thus explaining why luteolysis
and ovarian cyclicity can proceed in the absence of the uterus in primates. However, it remains to be established whether the
intraovarian process of luteolysis is mediated by arachidonic acid
and/or its metabolite PGF2
and whether the central
oxytocin pulse generator identified in nonprimate species plays a
mediatory role during luteolysis in primates. Regardless of the
mechanism, intraovarian luteolysis in primates (progesterone
withdrawal) appears to be the primary stimulus for the subsequent
production of endometrial prostaglandins associated with menstruation.
In contrast, luteolysis in nonprimate species appears to depend on the
prior production of endometrial prostaglandins. In primates, uterine
prostaglandin production may reflect a vestigial mechanism that has
been retained during evolution from an earlier dependence on uterine
prostaglandin production for luteolysis.
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T. A. Towle, P. C.W. Tsang, R. A. Milvae, M. K. Newbury, and J. A. McCracken Dynamic In Vivo Changes in Tissue Inhibitors of Metalloproteinases 1 and 2, and Matrix Metalloproteinases 2 and 9, During Prostaglandin F2{alpha}-Induced Luteolysis in Sheep Biol Reprod, May 1, 2002; 66(5): 1515 - 1521. [Abstract] [Full Text] |
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C. O. Stocco, L. F. Lau, and G. Gibori A Calcium/Calmodulin-dependent Activation of ERK1/2 Mediates JunD Phosphorylation and Induction of nur77 and 20alpha -hsd Genes by Prostaglandin F2alpha in Ovarian Cells J. Biol. Chem., January 25, 2002; 277(5): 3293 - 3302. [Abstract] [Full Text] [PDF] |
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A. Zetser, T. Kisliouk, E. Ivakin, and M. Lahav Dependence on Prolactin of the Luteolytic Effect of Prostaglandin F2{alpha} in Rat Luteal Cell Cultures Biol Reprod, October 1, 2001; 65(4): 1082 - 1091. [Abstract] [Full Text] [PDF] |
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J. Hu, T. E. Ludwig, U. Salli, F. Stormshak, and M. A. Mirando Autocrine/Paracrine Action of Oxytocin in Pig Endometrium Biol Reprod, June 1, 2001; 64(6): 1682 - 1688. [Abstract] [Full Text] |
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G. Gimpl and F. Fahrenholz The Oxytocin Receptor System: Structure, Function, and Regulation Physiol Rev, April 1, 2001; 81(2): 629 - 683. [Abstract] [Full Text] [PDF] |
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L. E. Anderson, Y.-L. Wu, S.-J. Tsai, and M. C. Wiltbank Prostaglandin F2{{alpha}} Receptor in the Corpus Luteum: Recent Information on the Gene, Messenger Ribonucleic Acid, and Protein Biol Reprod, April 1, 2001; 64(4): 1041 - 1047. [Abstract] [Full Text] |
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K. K. Olson, L. E. Anderson, M. C. Wiltbank, and D. H. Townson Actions of Prostaglandin F2{{alpha}} and Prolactin on Intercellular Adhesion Molecule-1 Expression and Monocyte/Macrophage Accumulation in the Rat Corpus Luteum Biol Reprod, March 1, 2001; 64(3): 890 - 897. [Abstract] [Full Text] |
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T. Engstrøm, P. Bratholm, N. J. Christensen, and H. Vilhardt Effect of Oxytocin Receptor Blockade on Rat Myometrial Responsiveness to Prostaglandin F2{alpha} Biol Reprod, November 1, 2000; 63(5): 1443 - 1449. [Abstract] [Full Text] |
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D. J. Skarzynski, S. Kobayashi, and K. Okuda Influence of Nitric Oxide and Noradrenaline on Prostaglandin F2{alpha}-Induced Oxytocin Secretion and Intracellular Calcium Mobilization in Cultured Bovine Luteal Cells Biol Reprod, October 1, 2000; 63(4): 1000 - 1005. [Abstract] [Full Text] |
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Y. Miyamoto, D. J. Skarzynski, and K. Okuda Is Tumor Necrosis Factor {alpha} a Trigger for the Initiation of Endometrial Prostaglandin F2{alpha} Release at Luteolysis in Cattle? Biol Reprod, May 1, 2000; 62(5): 1109 - 1115. [Abstract] [Full Text] |
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H. M. Fraser, S. E. Dickson, S. F. Lunn, C. Wulff, K. D. Morris, V. A. Carroll, and R. Bicknell Suppression of Luteal Angiogenesis in the Primate after Neutralization of Vascular Endothelial Growth Factor Endocrinology, March 1, 2000; 141(3): 995 - 1000. [Abstract] [Full Text] [PDF] |
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