| Circulating and placental endoglin concentrations in pregnancies complicated by intrauterine growth restriction and preeclampsia. | |
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MedLine Citation:
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PMID: 18462791 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Inadequate trophoblast invasion and spiral artery remodeling leading to poor placental perfusion and hypoxia are believed to underlie preeclampsia (PE) and intrauterine growth restriction (IUGR). Recent studies implicate increased circulating endoglin as a contributor to the pathogenesis of PE. The objective of this study was to determine whether placental and circulating endoglin concentrations are altered in pregnancies complicated by intrauterine growth restricted (IUGR) infants and to address the role of hypoxia on the regulation of placental endoglin. We analyzed 10 placentas each from normal pregnant (NP), PE, and IUGR subjects. Endoglin levels were 2.5-fold higher in preeclamptic placentas compared to NP (15.4+/-2.6 versus 5.7+/-1.0, p<0.01). In contrast, endoglin levels were similar in NP and IUGR placentas (5.7+/-1.0 vs 5.9+/-1.1, p=NS). Placentas from pregnancies with both PE and IUGR exhibited endoglin levels comparable to the PE group and significantly different from normotensive pregnancies with and without IUGR pregnancies (mean 14.9+/-4.0, n=9, p=0.013). Soluble endoglin concentrations in maternal plasma were comparable in NP and IUGR, but higher in women with PE (n=10 per group, p<0.05). Despite a 2-fold increase in hypoxia inducible factor, HIF-1alpha, we did not observe endoglin upregulation in NP, PE, or IUGR placental villous explants exposed to hypoxia (2% oxygen). In contrast to PE, placental or circulating endoglin is not increased in normotensive women delivering small, asymmetrically grown (IUGR) infants at term. The placentas of women with IUGR appear to be fundamentally different from PE women with respect to endoglin, despite the proposed common pathology of deficient trophoblast invasion/spiral artery remodeling and poor placental perfusion. |
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Authors:
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A Jeyabalan; S McGonigal; C Gilmour; C A Hubel; A Rajakumar |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural Date: 2008-05-06 |
Journal Detail:
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Title: Placenta Volume: 29 ISSN: 0143-4004 ISO Abbreviation: Placenta Publication Date: 2008 Jun |
Date Detail:
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Created Date: 2008-05-26 Completed Date: 2008-08-25 Revised Date: 2011-05-16 |
Medline Journal Info:
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Nlm Unique ID: 8006349 Medline TA: Placenta Country: England |
Other Details:
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Languages: eng Pagination: 555-63 Citation Subset: IM |
Affiliation:
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Department of Obstetrics and Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Antigens, CD / blood*, metabolism* Birth Weight Cells, Cultured Cohort Studies Female Fetal Growth Retardation / blood*, metabolism* Humans Infant, Newborn Organ Culture Techniques Placenta / metabolism* Pre-Eclampsia / blood*, metabolism* Pregnancy Receptors, Cell Surface / blood*, metabolism* Retrospective Studies |
| Grant Support | |
ID/Acronym/Agency:
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K12-HD043441-04/HD/NICHD NIH HHS; P01-HD30367/HD/NICHD NIH HHS; R03 HD055219-01/HD/NICHD NIH HHS; R03-HD055219/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD; 0/ENG protein, human; 0/Receptors, Cell Surface |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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