| The effect of leptin on mouse trophoblast cell invasion. | |
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MedLine Citation:
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PMID: 15306556 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The hormone leptin is produced by adipose tissue and can function as a signal of nutritional status to the reproductive system. The expression of leptin receptor and, in some species, leptin, in the placenta suggests a role for leptin in placental development, but this role has not been elucidated. Leptin is required at the time of embryo implantation in the leptin-deficient ob/ ob mouse and has been shown to upregulate expression of matrix metalloproteinases (MMPs), enzymes involved in trophoblast invasion, in cultured human trophoblast cells. This led us to the hypothesis that leptin promotes the invasiveness of trophoblast cells crucial to placental development. We found that leptin stimulated mouse trophoblast cell invasion through a matrigel-coated insert on Day 10, but not Day 18 of pregnancy. Optimal stimulation occurred at a concentration of 50 ng/ml leptin, similar to the peak plasma leptin concentration during pregnancy in the mouse. Leptin treatment did not stimulate proliferation of mouse trophoblast cells in primary culture. Leptin stimulation of invasion was prevented by 25 muM GM6001, an inhibitor of MMP activity. Our results suggest that leptin may play a role in the establishment of the placenta during early pregnancy and that this function is dependent on MMP activity. This effect of leptin may represent one mechanism by which body condition affects placental development. |
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Authors:
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Laura C Schulz; Eric P Widmaier |
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Publication Detail:
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Type: Journal Article Date: 2004-08-11 |
Journal Detail:
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Title: Biology of reproduction Volume: 71 ISSN: 0006-3363 ISO Abbreviation: Biol. Reprod. Publication Date: 2004 Dec |
Date Detail:
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Created Date: 2004-11-23 Completed Date: 2005-04-14 Revised Date: 2011-05-06 |
Medline Journal Info:
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Nlm Unique ID: 0207224 Medline TA: Biol Reprod Country: United States |
Other Details:
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Languages: eng Pagination: 1963-7 Citation Subset: IM |
Affiliation:
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Department of Biology, Boston University, Boston, Massachusetts 02215, USA. lcschulz@bu.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Biocompatible Materials Cell Division / drug effects Cell Movement / drug effects, physiology* Cells, Cultured Collagen Dipeptides / pharmacology Drug Combinations Immunohistochemistry Laminin Leptin / pharmacology, physiology* Matrix Metalloproteinases / antagonists & inhibitors, physiology Membranes, Artificial Mice Protease Inhibitors / pharmacology Proteoglycans Recombinant Proteins / pharmacology Trophoblasts / cytology, drug effects, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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F32 HD045116-02/HD/NICHD NIH HHS; R00 HD055231-05/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Biocompatible Materials; 0/Dipeptides; 0/Drug Combinations; 0/GM 6001; 0/Laminin; 0/Leptin; 0/Membranes, Artificial; 0/Protease Inhibitors; 0/Proteoglycans; 0/Recombinant Proteins; 119978-18-6/matrigel; 9007-34-5/Collagen; EC 3.4.24.-/Matrix Metalloproteinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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