Document Detail


System A activity and vascular function in the placental-specific Igf2 knockout mouse.
MedLine Citation:
PMID:  21851977     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: Deletion of the placental-specific P0 transcript of the insulin-like growth factor gene (Igf2) reduces placental growth from early pregnancy onwards. In Igf2 P0 knockout fetuses (P0), maternofetal flux of (14)C-methylaminoisobutyric acid ((14)C-MeAIB) mediated by system A amino acid transporter activity is increased at embryonic day 16 (E16), but this stimulation is not sustained, and by E19, fetal growth restriction (FGR) ensues. Here, we investigated whether upregulated (14)C-MeAIB transfer does occur concomitantly with a change in System A amino acid transporter activity and whether altered uteroplacental vascular function contributes to the FGR. We tested the hypothesis that FGR in P0 mice is attributable to altered nutrient transport rather than aberrant uteroplacental vascular function.
METHODS: Plasma membrane vesicles were isolated from placentas of P0 and wild-type (WT) fetuses at E16 and E19. System A amino acid transporter activity was measured as sodium-dependent (14)C-MeAIB uptake over 60s. Wire myography was performed on uterine artery branches supplying P0 or WT implantation sites and agonist-induced constriction and dilation measured.
RESULTS: Sodium-dependent uptake of (14)C-MeAIB (at 60s) was significantly (P < 0.05) higher in P0 compared to WT vesicles at E16; at E19 (14)C-MeAIB uptake was similar between P0 and WT. Uterine artery branch vascular reactivity was comparable between groups.
CONCLUSIONS: System A activity in the maternal-facing plasma membrane of syncytiotrophoblast layer II underpins the adaptations observed in the transplacental MeAIB flux of P0 mice. Unaltered uterine artery vascular function suggests that the FGR phenotype of P0 fetuses is primarily due to deficient placental nutrient exchange capacity.
Authors:
L C Kusinski; M R Dilworth; P N Baker; C P Sibley; M Wareing; J D Glazier
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-08-17
Journal Detail:
Title:  Placenta     Volume:  32     ISSN:  1532-3102     ISO Abbreviation:  Placenta     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-07     Completed Date:  2012-03-06     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  8006349     Medline TA:  Placenta     Country:  England    
Other Details:
Languages:  eng     Pagination:  871-6     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ltd. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Transport System A / metabolism*,  physiology
Animals
Biological Transport
Blood Vessels / metabolism,  physiology*
Cell Fractionation
Female
Insulin-Like Growth Factor II / genetics*,  metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Organ Specificity / genetics
Placenta / blood supply,  metabolism*
Placental Circulation / genetics,  physiology
Pregnancy
Uterine Artery / metabolism,  physiology
beta-Alanine / analogs & derivatives,  pharmacokinetics
Grant Support
ID/Acronym/Agency:
92495//Medical Research Council; G0802770//Medical Research Council; //Biotechnology and Biological Sciences Research Council
Chemical
Reg. No./Substance:
0/Amino Acid Transport System A; 0/IGF2 protein, mouse; 11P2JDE17B/beta-Alanine; 19036-43-2/2,2-dimethyl-beta-alanine; 67763-97-7/Insulin-Like Growth Factor II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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