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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-09-0109v1 JOE-09-0109v2 202/3/407    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Chen, Y. Articles by Pepling, M. E PubMed PubMed Citation Articles by Chen, Y. Articles by Pepling, M. E

Department of Biology, Syracuse University, 107 College Place, Syracuse, New York 13244, USA

(Correspondence should be addressed to M E Pepling; Email: mepeplin{at}syr.edu)

During mouse embryonic development, oocytes develop in germline cysts, formed by several rounds of cell division followed by incomplete cytokinesis. Shortly after birth, cysts break down and individual oocytes are enclosed by granulosa cells to form primordial follicles. At the same time, two-thirds of the oocytes die by apoptosis with only one-third surviving. We have previously shown that the steroid hormones, estradiol (E₂), and progesterone as well as the phytoestrogen genistein can inhibit cyst breakdown and primordial follicle assembly. However, the mechanisms by which steroid hormones regulate oocyte cyst breakdown and selective oocyte survival are unknown. Here, we confirmed the expression of estrogen receptor (ER) mRNA and protein in neonatal mouse ovaries using reverse transcriptase-PCR, western blotting, and immunocytochemistry. We then used ER-specific agonists and antagonists to understand the mechanism of estrogen signaling. 4,4',4''-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol, an ER-selective agonist, and 2,3-bis(4-hydroxyphenyl)-propionitrile, an ERβ-selective agonist, both inhibited cyst breakdown in organ culture, suggesting that E₂ can signal through both the receptors to regulate cyst breakdown. ICI 182,780, an ER antagonist, completely blocked E₂'s action. 1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride, an ER-specific antagonist, fully blocked E₂'s effect on oocyte cyst breakdown and primordial follicle assembly and (R,R)-5,11-diethyl-5,6,11,12-tetrahydro-2,8-chrysenediol, an ERβ-specific antagonist, partially blocked E₂, further supporting the idea that both receptors are involved in estrogen signaling in neonatal oocyte development. E₂ conjugated to BSA, which can only exert effects at the membrane, was able to inhibit cyst breakdown, implying that E₂ could also function through a membrane-bound ER to regulate cyst breakdown.

This article has been cited by other articles:

				M. E Pepling, E. A Sundman, N. L Patterson, G. W Gephardt, L. Medico Jr, and K. I Wilson Differences in oocyte development and estradiol sensitivity among mouse strains Reproduction, February 1, 2010; 139(2): 349 - 357. [Abstract] [Full Text] [PDF]