| Hypertension produced by placental ischemia in pregnant rats is associated with increased soluble endoglin expression. | |
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MedLine Citation:
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PMID: 19075097 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Recent clinical studies indicate that an excess of angiostatic factors, such as soluble endoglin (sEng), is related to the occurrence of preeclampsia. Although recent clinical studies report that sEng is increased in preeclamptic women, the mechanisms underlying its overexpression remain unclear. Evidence suggests that hypoxia and induction of heme oxygenase-1 have opposing effects on sEng expression, the former stimulatory and the latter inhibitory. Hence, we hypothesized that placental ischemia because of reduced uterine perfusion pressure (RUPP) in the pregnant rat would increase sEng expression and decrease heme oxygenase-1. Mean arterial pressure was obtained via arterial catheter, and serum and placental proteins were measured by Western blot. Mean arterial pressure was increased (132+/-3 mm Hg versus 102+/-2 mm Hg; P<0.001), and fetal (2.35+/-0.05 g versus 1.76+/-0.08 g; P<0.001) and placental weight were decreased (0.47+/-0.04 g versus 0.58+/-0.03 g; P<0.01) in the RUPP compared with normal pregnant controls. Serum sEng (0.10+/-0.02 arbitrary pixel units [apu] versus 0.05+/-0.01 apu; P<0.05) and placental endoglin (4.7+/-2.3 apu versus 1.45+/-0.42 apu; P<0.05) were increased along with placental hypoxia inducible factor-1 alpha (1.42+/-0.25 apu versus 0.68+/-0.09 apu; P<0.05) expression in the RUPP versus the normal pregnant dams. Placental HO-1 (1.4+/-0.3 apu versus 2.5+/-0.1 apu; P<0.05) expression decreased in the RUPP compared with normal pregnant dams. The present findings support our hypothesis that placental ischemia because of RUPP increases the expression of sEng and shifts the balance of angiogenic factors in the maternal circulation toward an angiostatic state. The present study provides further evidence that placental ischemia is a strong in vivo stimulus of angiostatic factors during pregnancy. |
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Authors:
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Jeffrey S Gilbert; Sara A B Gilbert; Marietta Arany; Joey P Granger |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2008-12-15 |
Journal Detail:
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Title: Hypertension Volume: 53 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2009 Feb |
Date Detail:
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Created Date: 2009-01-23 Completed Date: 2009-02-13 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 399-403 Citation Subset: IM |
Affiliation:
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Department of Physiology, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216-4505, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure / physiology Disease Models, Animal Female Heme Oxygenase-1 / metabolism Hypertension / metabolism*, physiopathology Hypoxia-Inducible Factor 1, alpha Subunit / metabolism Intracellular Signaling Peptides and Proteins / metabolism* Ischemia / metabolism* Placenta / blood supply* Pre-Eclampsia / etiology, metabolism Pregnancy Pregnancy, Animal / metabolism* Rats Rats, Sprague-Dawley |
| Grant Support | |
ID/Acronym/Agency:
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F32 HL090269-01/HL/NHLBI NIH HHS; HL51971/HL/NHLBI NIH HHS; HL90269/HL/NHLBI NIH HHS; P01 HL051971-165259/HL/NHLBI NIH HHS; R01 HL038499-18/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Hif1a protein, rat; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/Intracellular Signaling Peptides and Proteins; 0/endoglin protein, rat; EC 1.14.99.3/Heme Oxygenase-1 |
| Comments/Corrections | |
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