Source:http://linkedlifedata.com/resource/pubmed/id/15687332
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0019932,
umls-concept:C0024429,
umls-concept:C0036536,
umls-concept:C0036537,
umls-concept:C0086418,
umls-concept:C0220781,
umls-concept:C0227843,
umls-concept:C0312359,
umls-concept:C0442805,
umls-concept:C0871261,
umls-concept:C1141639,
umls-concept:C1334507,
umls-concept:C1704632,
umls-concept:C1706089,
umls-concept:C1706817,
umls-concept:C1883254,
umls-concept:C2911692
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| pubmed:issue |
5
|
| pubmed:dateCreated |
2005-5-5
|
| pubmed:abstractText |
Originally identified for its capacity to inhibit the random migration of macrophages in vitro, macrophage migration inhibitory factor (MIF) is now recognized as a multifunctional cytokine that modulates the immune response and acts as a growth and angiogenic factor. Recent studies showed that MIF is expressed in the human endometrium across the menstrual cycle as well as in chorionic villi from first-trimester human placenta, which suggests an involvement of MIF in reproduction. Herein, we report that human chorionic gonadotropin (hCG), a glycoprotein hormone that plays a critical role in the initiation and maintenance of pregnancy, markedly stimulates MIF expression in endometrial stromal cells. Cell treatment with hCG resulted in a dose-dependent increase in MIF protein secretion and mRNA steady-state levels, as shown by immunocytochemistry, ELISA, and RT-PCR. Assessment of MIF mRNA half-life showed that hCG treatment had no significant effect on MIF mRNA stability (P = 0.08). However, nuclear transcription assays (run-on) revealed that hCG acts predominantly by up-regulating MIF gene transcription. These data clearly indicate that MIF can mediate hCG effects on the human endometrium and, in view of the immunomodulatory and angiogenic properties of MIF, reveal a new mechanism by which hCG sustains human pregnancy and promotes embryonic growth.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
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| pubmed:issn |
0021-972X
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
90
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
2904-10
|
| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:15687332-Adult,
pubmed-meshheading:15687332-Cells, Cultured,
pubmed-meshheading:15687332-Chorionic Gonadotropin,
pubmed-meshheading:15687332-Endometrium,
pubmed-meshheading:15687332-Female,
pubmed-meshheading:15687332-Humans,
pubmed-meshheading:15687332-Macrophage Migration-Inhibitory Factors,
pubmed-meshheading:15687332-RNA, Messenger
|
| pubmed:year |
2005
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| pubmed:articleTitle |
Marked increase in macrophage migration inhibitory factor synthesis and secretion in human endometrial cells in response to human chorionic gonadotropin hormone.
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| pubmed:affiliation |
Unité d'Endocrinologie de la Reproduction, Laboratoire d'Endocrinologie de la Reproduction, Centre de Recherche, Hôpital Saint-François d'Assise, 10 rue de l'Espinay, Local D0-711, Québec, Québec, Canada G1L 3L5. ali.akoum@crsfa.ulaval.ca
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|