| Differential triiodothyronine responsiveness and transport by human cytotrophoblasts from normal and growth-restricted pregnancies. | |
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MedLine Citation:
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PMID: 20660035 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: Abnormal placentation in human pregnancy is associated with intrauterine fetal growth restriction (IUGR). Our group has previously reported the association between severe IUGR, lower fetal circulating concentrations of thyroid hormones (THs), and altered expression of TH receptors and TH transporters within human placental villi. We postulate that altered TH bioavailability to trophoblasts may contribute to the pathogenesis of IUGR. DESIGN AND OBJECTIVE: Cytotrophoblasts were isolated from normal and IUGR human placentae to compare their responsiveness to T(3) and their capability for T(3) transport. RESULTS: Compared with normal cytotrophoblasts, the viability of IUGR cytotrophoblasts (assessed by methyltetrazoleum assay) was significantly reduced (P < 0.001), whereas apoptosis (assessed using caspase 3/7 activity and M30 immunoreactivity) was significantly increased after T(3) treatment for 48 h (P < 0.001 and P < 0.01, respectively). The secretion of human chorionic gonadotropin was significantly increased by IUGR cytotrophoblasts compared with normal cytotrophoblasts (P < 0.001), independently of T(3) treatment. Net transport of [(125)I]T(3) was 20% higher by IUGR cytotrophoblasts compared with normal cytotrophoblasts (P < 0.001), and this was accompanied by a 2-fold increase in the protein expression of the TH transporter, monocarboxylate transporter 8, as assessed by Western immunoblotting (P < 0.01). CONCLUSIONS: IUGR cytotrophoblasts demonstrate altered responsiveness to T(3) with significant effects on cell survival and apoptosis compared with normal cytotrophoblasts. Increased monocarboxylate transporter 8 expression and intracellular T(3) accumulation may contribute to the altered T(3) responsiveness of IUGR cytotrophoblasts. |
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Authors:
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E Vasilopoulou; L S Loubière; A Martín-Santos; C J McCabe; J A Franklyn; M D Kilby; S-Y Chan |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2010-07-21 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 95 ISSN: 1945-7197 ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-10-07 Completed Date: 2010-11-15 Revised Date: 2011-07-26 |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: 4762-70 Citation Subset: AIM; IM |
Affiliation:
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School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Amino Acid Transport Systems, Neutral / genetics, metabolism Apoptosis / drug effects Biological Transport / physiology Cell Survival / drug effects Cells, Cultured Chorionic Gonadotropin / secretion Female Fetal Growth Retardation / metabolism, pathology* Humans Male Monocarboxylic Acid Transporters / genetics, metabolism Placenta / metabolism, pathology Pregnancy Triiodothyronine / metabolism*, pharmacokinetics, pharmacology* Trophoblasts / drug effects*, metabolism*, pathology Young Adult |
| Grant Support | |
ID/Acronym/Agency:
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G0501548//Medical Research Council; G0600285//Department of Health |
| Chemical | |
Reg. No./Substance:
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0/Amino Acid Transport Systems, Neutral; 0/Chorionic Gonadotropin; 0/Monocarboxylic Acid Transporters; 0/SLC16A10 protein, human; 0/SLC16A2 protein, human; 6893-02-3/Triiodothyronine |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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