rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2000-6-2
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pubmed:abstractText |
Apoptosis in corpus luteum (CL) is induced by prolactin (PRL) in female rats. PRL-induced apoptosis in CL is mediated by the Fas/Fas ligand (FasL) system. The CL consists of steroidogenic and non-steroidogenic cells, including immunocytes. Fas mRNA was detected only in the luteal steroidogenic cells, and FasL mRNA was expressed only by the non-steroidogenic CD3-positive luteal immunocytes. Removing the luteal immune cells from the luteal cells inhibited PRL-induced luteal cell apoptosis effectively. Thus, FasL-expressing non-steroidogenic luteal immunocytes are required for PRL-induced luteal cell apoptosis and heterogeneous induction of apoptosis by Fas/FasL in CL.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Apr
|
pubmed:issn |
0014-5793
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
21
|
pubmed:volume |
472
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
137-42
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10781821-Animals,
pubmed-meshheading:10781821-Antigens, CD3,
pubmed-meshheading:10781821-Antigens, CD95,
pubmed-meshheading:10781821-Apoptosis,
pubmed-meshheading:10781821-Blotting, Western,
pubmed-meshheading:10781821-Corpus Luteum,
pubmed-meshheading:10781821-Fas Ligand Protein,
pubmed-meshheading:10781821-Female,
pubmed-meshheading:10781821-Killer Cells, Natural,
pubmed-meshheading:10781821-Ligands,
pubmed-meshheading:10781821-Membrane Glycoproteins,
pubmed-meshheading:10781821-Prolactin,
pubmed-meshheading:10781821-Rats,
pubmed-meshheading:10781821-Rats, Wistar,
pubmed-meshheading:10781821-Reverse Transcriptase Polymerase Chain Reaction
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pubmed:year |
2000
|
pubmed:articleTitle |
Requirement of the Fas ligand-expressing luteal immune cells for regression of corpus luteum.
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pubmed:affiliation |
Department of Veterinary Physiology, Veterinary Medical Science, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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