Biol Reprod Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


BOR - Papers in Press, published online ahead of print January 14, 2004.
Biol Reprod 2004, 10.1095/biolreprod.103.020461
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
70/5/1333    most recent
biolreprod.103.020461v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Diaz, F. J.
Right arrow Articles by Wiltbank, M. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Diaz, F. J.
Right arrow Articles by Wiltbank, M. C.
Agricola
Right arrow Articles by Diaz, F. J.
Right arrow Articles by Wiltbank, M. C.
BIOLOGY OF REPRODUCTION 70, 1333–1339 (2004)
DOI: 10.1095/biolreprod.103.020461
© 2004 by the Society for the Study of Reproduction, Inc.


Ovary

Acquisition of Luteolytic Capacity: Changes in Prostaglandin F2{alpha} Regulation of Steroid Hormone Receptors and Estradiol Biosynthesis in Pig Corpora Lutea1

Francisco J. Diaz, and Milo C. Wiltbank2

Endocrinology-Reproductive Physiology Program and Department of Dairy Science, University of Wisconsin-Madison, Madison, Wisconsin 53706

The pig corpora lutea (CL) acquires luteolytic capacity at about Day 13 of the estrous cycle, after which luteolysis occurs in response to prostaglandin F2{alpha} (PGF2{alpha}) treatment. We postulated that differences in transcription factors such as the steroid hormone receptors may be responsible for the differences in PGF2{alpha}-induced gene expression after acquisition of luteolytic capacity. In these studies, we evaluated the effect of PGF2{alpha} on luteal expression of receptors for progesterone (nuclear and membrane progesterone receptor [PR]), estradiol (ER{alpha} and ERß), glucocorticoid, androgens, and two enzymes in estradiol synthesis (P450-17{alpha} and aromatase). Two experiments were conducted to examine the early (0.5 h, experiment I) and late (10 h, experiment II) effects of PGF2{alpha} on the expression of these receptors in CL with (Day 17) or without (Day 9) luteolytic capacity. PGF2{alpha} decreased ER{alpha} mRNA (35%) and increased ERß mRNA (558%) and protein (376%) only in Day 17 CL and not Day 9. The estradiol biosynthetic pathway was upregulated by PGF2{alpha} in Day 17 CL but not Day 9 CL, with a dramatic increase in aromatase mRNA and luteal estradiol content. Nuclear PR was not affected by PGF2{alpha}, but was greater (176%) in Day 9 CL, while a putative membrane PR was greater (156%) in Day 17 than Day 9 CL. There were no detectable changes in glucocorticoid or androgen receptor mRNA. Thus, luteolytic capacity is associated with upregulation of estradiol biosynthesis, which in conjunction with increased ERß expression and altered PR expression may promote luteolysis in the pig CL.

1 Supported by USDA-00-35203-9134, HD-32623, and an Advanced Opportunity Fellowship to F.J.D.

2 Correspondence: Milo C. Wiltbank, Department of Dairy Science, University of Wisconsin-Madison, 1675 Observatory Drive, Madison, WI 53706. FAX: 608 263 9412; wiltbank{at}calshp.cals.wisc.edu




This article has been cited by other articles:


Home page
Biol. Reprod.Home page
J. J. Peluso
Multiplicity of Progesterone's Actions and Receptors in the Mammalian Ovary
Biol Reprod, July 1, 2006; 75(1): 2 - 8.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
C. Stocco
In Vivo and in Vitro Inhibition of cyp19 Gene Expression by Prostaglandin F2{alpha} in Murine Luteal Cells: Implication of GATA-4
Endocrinology, November 1, 2004; 145(11): 4957 - 4966.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by the Society for the Study of Reproduction.