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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1997-1-21
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pubmed:abstractText |
The effects of recombinant ovine interferon-tau (IFN-tau) and progesterone on oestrogen-stimulated expression of endometrial receptors for oestrogen (ER), progesterone (PR) and oxytocin (OTR) were determined in ovariectomized ewes. Cyclic ewes (n = 16) were ovariectomized and fitted with uterine catheters on Day 4 of the oestrous cycle (Day O, oestrous) and assigned randomly in 2 x 2-factorial arrangement to receive daily intrauterine injections of either recombinant ovine IFN-tau (roIFN-tau; 2 x 10(7) anti-viral units) or control proteins from Day 11 to Day 15 and 50 mg progesterone from either Day 4 to Day 10 (E-P) or Day 4 to Day 15 (E+P). All ewes received 50 micrograms oestradiol-17 beta on Days 13, 14 and 15 and were hysterectomized on Day 16. In control ewes, endometrial ER mRNA, PR protein and OTR density were greater in E-P- than E+P- treated ewes. In E-P ewes, roIFN-tau decreased oestrogen-stimulated increases in ER and OTR, but not PR expression compared with control ewes. In E+P ewes, endometrial ER mRNA and protein, PR mRNA and protein, and OTR levels were lower in roIFN-tau-treated ewes than control ewes. Immunoreactive ER and PR were absent in the endometrial luminal and superficial glandular epithelium of roIFN-tau compared with control ewes, but were present in the deep glandular epithelium and stroma regardless of steroid or protein treatment. These results indicate that progesterone affects oestrogen-induced increases in endometrial ER, PR and OTR expression in the PR+ deep glandular epithelium and stroma, whereas IFN-tau suppresses oestrogen-induced increases ER, PR and OTR expression in the PR- luminal and superficial glandular epithelium. These combined actions of IFN-tau and progesterone to suppress oestrogen-induced increases in endometrial OTR formation would prevent pulsatile production of luteolytic prostaglandin F2 alpha by the endometrium during early pregnancy.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Estradiol,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Pregnancy Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Progesterone,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Estrogen,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Oxytocin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Progesterone,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/trophoblastin
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pubmed:status |
MEDLINE
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pubmed:issn |
1031-3613
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
843-53
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8876043-Animals,
pubmed-meshheading:8876043-Endometrium,
pubmed-meshheading:8876043-Estradiol,
pubmed-meshheading:8876043-Female,
pubmed-meshheading:8876043-Gene Expression Regulation,
pubmed-meshheading:8876043-Humans,
pubmed-meshheading:8876043-Immunohistochemistry,
pubmed-meshheading:8876043-Interferon Type I,
pubmed-meshheading:8876043-Ovariectomy,
pubmed-meshheading:8876043-Pregnancy Proteins,
pubmed-meshheading:8876043-Progesterone,
pubmed-meshheading:8876043-Random Allocation,
pubmed-meshheading:8876043-Receptors, Estrogen,
pubmed-meshheading:8876043-Receptors, Oxytocin,
pubmed-meshheading:8876043-Receptors, Progesterone,
pubmed-meshheading:8876043-Recombinant Proteins,
pubmed-meshheading:8876043-Sheep
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pubmed:year |
1996
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pubmed:articleTitle |
Effects of interferon-tau and progesterone on oestrogen-stimulated expression of receptors for oestrogen, progesterone and oxytocin in the endometrium of ovariectomized ewes.
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pubmed:affiliation |
Department of Animal Science, Texas A&M University, College Station 77843-2471, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.
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