Source:http://linkedlifedata.com/resource/pubmed/id/10566679
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
1999-11-26
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pubmed:abstractText |
The present investigation examined the effect of interleukin-1beta (IL-1beta) on progesterone production by human luteal cells and the expression and localization of the IL-1 system in the human corpus luteum (CL). Luteal cells were isolated from corpora lutea collected throughout the luteal phase. After dispersion, luteal cells were treated with a panel of monoclonal antibodies directed to leukocyte-specific molecules. The leukocytes were isolated with immunomagnetic beads. Leukocyte-free luteal cells exhibited greater steroidogenic responsiveness to hCG toward the end of the luteal phase. The treatment of mixed luteal cells (total luteal cells) with IL-1beta inhibited by 60% hCG-stimulated progesterone production. Interestingly, the treatment of leukocyte-free luteal cells with IL-1beta did not affect progesterone production. In addition, the treatment of mixed luteal cells with monoclonal antibodies against IL-1 receptor type I (IL-1RtI) resulted in a 2.5-fold increase in the hCG-supported progesterone production. IL-1RtI and IL-1 receptor antagonist were localized by immunohistochemistry in both somatic and immune cells of the CL. Flow cytometric analysis indicated that both nonleukocyte luteal cells and leukocyte-luteal cells exhibited IL-1Rt-I positive cells, representing 56% and 31% of the total luteal cells, respectively. However, 13% of nonleukocyte luteal cells did not express IL-1Rt-I. Northern analysis demonstrated the presence of the 5.1-kb IL-1RtI messenger ribonucleic acid transcript in CL of different ages. RT-PCR indicated that both leukocyte-free luteal cells and luteal leukocytes express IL-1RtI messenger ribonucleic acid. We conclude that 1) luteal leukocytes have an inhibitory effect on hCG-stimulated progesterone production; 2) IL-1beta inhibits hCG-stimulated progesterone production only in mixed luteal cell cultures, indicating that leukocytes mediate the effect; 3) the somatic and immune cells of the CL are sites of action and expression of the IL-1 system; and 4) interaction between the steroidogenic and immune cells of the CL suggests a functional intraovarian role for IL-1beta in CL physiology.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Chorionic Gonadotropin,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Progesterone,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0021-972X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
84
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4239-45
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10566679-Adult,
pubmed-meshheading:10566679-Antibodies, Monoclonal,
pubmed-meshheading:10566679-Chorionic Gonadotropin,
pubmed-meshheading:10566679-Corpus Luteum,
pubmed-meshheading:10566679-Female,
pubmed-meshheading:10566679-Flow Cytometry,
pubmed-meshheading:10566679-Humans,
pubmed-meshheading:10566679-Immunohistochemistry,
pubmed-meshheading:10566679-Interleukin-1,
pubmed-meshheading:10566679-Kinetics,
pubmed-meshheading:10566679-Leukocytes,
pubmed-meshheading:10566679-Luteal Cells,
pubmed-meshheading:10566679-Luteal Phase,
pubmed-meshheading:10566679-Progesterone,
pubmed-meshheading:10566679-RNA, Messenger,
pubmed-meshheading:10566679-Receptors, Interleukin-1,
pubmed-meshheading:10566679-Reverse Transcriptase Polymerase Chain Reaction
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pubmed:year |
1999
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pubmed:articleTitle |
Interleukin-1beta (IL-1beta) is a modulator of human luteal cell steroidogenesis: localization of the IL type I system in the corpus luteum.
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pubmed:affiliation |
Institute of Maternal and Child Research, School of Medicine and Department of Obstetrics and Gynecology, University of Chile, Santiago.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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