| Uterine artery remodeling and reproductive performance are impaired in endothelial nitric oxide synthase-deficient mice. | |
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MedLine Citation:
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PMID: 15659709 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The progressive rise in uterine blood flow during pregnancy is accompanied by outward hypertrophic remodeling of the uterine artery (UA). This process involves changes of the arterial smooth muscle cells and extracellular matrix. Acute increases in blood flow stimulate endothelial production of nitric oxide (NO). It remains to be established whether endothelial NO synthase (eNOS) is involved in pregnancy-related arterial remodeling. We tested the hypothesis that absence of eNOS results in a reduced remodeling capacity of the UA during pregnancy leading to a decline in neonatal outcome. UA of nonpregnant and pregnant wild-type (Nos3+/+) and eNOS-deficient (Nos3-/-) mice were collected and processed for standard morphometrical analyses. In addition, cross sections of UA were processed for cytological (smoothelin, smooth muscle alpha-actin) and proliferation (Ki-67) immunostaining. We compared the pregnancy-related changes longitudinally and, together with the data on pregnancy outcome, transversally by analysis of variance with Bonferroni correction. During pregnancy, the increases in radius and medial cross sectional area of Nos3-/- UA was significantly less than those of Nos3+/+ UA. Smooth muscle cell dedifferentiation and proliferation were impaired in gravid Nos3-/- mice as deduced from the lack of change in the expression of smoothelin and smooth muscle alpha-actin, and the reduced Ki-67 expression. Until 17 days of gestation, litter size did not differ between both genotypes, but at birth the number of viable newborn pups and their weights were smaller in Nos3-/- than in Nos3+/+ mice. We conclude that absence of eNOS adversely affects UA remodeling in pregnancy, which may explain the impaired pregnancy outcome observed in these mice. |
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Authors:
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Olivier W H van der Heijden; Yvonne P G Essers; Gregorio Fazzi; Louis L H Peeters; Jo G R De Mey; Guillaume J J M van Eys |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2005-01-19 |
Journal Detail:
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Title: Biology of reproduction Volume: 72 ISSN: 0006-3363 ISO Abbreviation: Biol. Reprod. Publication Date: 2005 May |
Date Detail:
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Created Date: 2005-04-21 Completed Date: 2005-09-19 Revised Date: 2006-11-15 |
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: 1161-8 Citation Subset: IM |
Affiliation:
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Department of Obstetrics and Gynecology, University of Maastricht, The Netherlands. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptation, Physiological Animals Animals, Newborn Arteries / anatomy & histology, enzymology, physiology Female Gestational Age Mice Mice, Inbred C57BL Mice, Knockout Nitric Oxide Synthase / deficiency*, genetics Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III Pregnancy Pregnancy Outcome Reproduction Uterus / blood supply*, enzymology* |
| Chemical | |
Reg. No./Substance:
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EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse |
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