Linked Life Data

19505948

Source:http://linkedlifedata.com/resource/pubmed/id/19505948

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-8-19
pubmed:abstractText
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 (E(2)), 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 alpha-selective agonist, and 2,3-bis(4-hydroxyphenyl)-propionitrile, an ER beta-selective agonist, both inhibited cyst breakdown in organ culture, suggesting that E(2) can signal through both the receptors to regulate cyst breakdown. ICI 182,780, an ER antagonist, completely blocked E(2)'s action. 1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride, an ER alpha-specific antagonist, fully blocked E(2)'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 ER beta-specific antagonist, partially blocked E(2), further supporting the idea that both receptors are involved in estrogen signaling in neonatal oocyte development. E(2) conjugated to BSA, which can only exert effects at the membrane, was able to inhibit cyst breakdown, implying that E(2) could also function through a membrane-bound ER to regulate cyst breakdown.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1479-6805
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
202
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
407-17
pubmed:meshHeading
pubmed-meshheading:19505948-Animals, pubmed-meshheading:19505948-Animals, Newborn, pubmed-meshheading:19505948-Estradiol, pubmed-meshheading:19505948-Estrogen Antagonists, pubmed-meshheading:19505948-Estrogen Receptor alpha, pubmed-meshheading:19505948-Estrogen Receptor beta, pubmed-meshheading:19505948-Estrogens, pubmed-meshheading:19505948-Female, pubmed-meshheading:19505948-Genistein, pubmed-meshheading:19505948-Male, pubmed-meshheading:19505948-Mice, pubmed-meshheading:19505948-Mice, Inbred Strains, pubmed-meshheading:19505948-NAD, pubmed-meshheading:19505948-Oocytes, pubmed-meshheading:19505948-Organ Culture Techniques, pubmed-meshheading:19505948-Ovarian Follicle, pubmed-meshheading:19505948-Phytoestrogens, pubmed-meshheading:19505948-Pregnancy, pubmed-meshheading:19505948-RNA, Messenger, pubmed-meshheading:19505948-Signal Transduction
pubmed:year
2009
pubmed:articleTitle
Estrogen can signal through multiple pathways to regulate oocyte cyst breakdown and primordial follicle assembly in the neonatal mouse ovary.
pubmed:affiliation
Department of Biology, Syracuse University, 107 College Place, Syracuse, New York 13244, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.