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Statements

Subject Item
n2:RIV%2F00216208%3A11110%2F13%3A10188753%21RIV14-MSM-11110___
rdf:type
skos:Concept n17:Vysledek
rdfs:seeAlso
http://dx.doi.org/10.1016/j.yjmcc.2013.04.015
dcterms:description
Cardiovascular malformations are the most common manifestation of diabetic embryopathy. The molecular mechanisms underlying the teratogenic effect of maternal diabetes have not been fully elucidated. Using genome-wide expression profiling, we previously demonstrated that exposure to maternal diabetes resulted in dysregulation of the hypoxia-inducible factor 1 (HIF-1) pathway in the developing embryo. We thus considered a possible link between HIF-1-regulated pathways and the development of congenital malformations. HIF-1 alpha heterozygous-null (Hif1a(+/-)) and wild type (Wt) littermate embryos were exposed to the intrauterine environment of a diabetic mother to analyze the frequency and morphology of congenital defects, and assess gene expression changes in Wt and Hif1a(+/-) embryos. We observed a decreased number of embryos per litter and an increased incidence of heart malformations, including atrioventricular septal defects and reduced myocardial mass, in diabetes-exposed Hif1a(+/-) embryos as compared to Wt embryos. We also detected significant differences in the expression of key cardiac transcription factors, including Nkx2.5, Tbx5, and Mef2C, in diabetes-exposed Hif1a(+/-) embryonic hearts compared to Wt littermates. Thus, partial global HIF-1 alpha deficiency alters gene expression in the developing heart and increases susceptibility to congenital defects in a mouse model of diabetic pregnancy. Cardiovascular malformations are the most common manifestation of diabetic embryopathy. The molecular mechanisms underlying the teratogenic effect of maternal diabetes have not been fully elucidated. Using genome-wide expression profiling, we previously demonstrated that exposure to maternal diabetes resulted in dysregulation of the hypoxia-inducible factor 1 (HIF-1) pathway in the developing embryo. We thus considered a possible link between HIF-1-regulated pathways and the development of congenital malformations. HIF-1 alpha heterozygous-null (Hif1a(+/-)) and wild type (Wt) littermate embryos were exposed to the intrauterine environment of a diabetic mother to analyze the frequency and morphology of congenital defects, and assess gene expression changes in Wt and Hif1a(+/-) embryos. We observed a decreased number of embryos per litter and an increased incidence of heart malformations, including atrioventricular septal defects and reduced myocardial mass, in diabetes-exposed Hif1a(+/-) embryos as compared to Wt embryos. We also detected significant differences in the expression of key cardiac transcription factors, including Nkx2.5, Tbx5, and Mef2C, in diabetes-exposed Hif1a(+/-) embryonic hearts compared to Wt littermates. Thus, partial global HIF-1 alpha deficiency alters gene expression in the developing heart and increases susceptibility to congenital defects in a mouse model of diabetic pregnancy.
dcterms:title
Increased susceptibility of HIF-1 alpha heterozygous-null mice to cardiovascular malformations associated with maternal diabetes Increased susceptibility of HIF-1 alpha heterozygous-null mice to cardiovascular malformations associated with maternal diabetes
skos:prefLabel
Increased susceptibility of HIF-1 alpha heterozygous-null mice to cardiovascular malformations associated with maternal diabetes Increased susceptibility of HIF-1 alpha heterozygous-null mice to cardiovascular malformations associated with maternal diabetes
skos:notation
RIV/00216208:11110/13:10188753!RIV14-MSM-11110___
n17:predkladatel
n19:orjk%3A11110
n3:aktivita
n8:V n8:Z n8:P n8:I
n3:aktivity
I, P(GA301/09/0117), P(GAP302/11/1308), V, Z(AV0Z50520701)
n3:cisloPeriodika
JUL
n3:dodaniDat
n21:2014
n3:domaciTvurceVysledku
n5:5754623
n3:druhVysledku
n13:J
n3:duvernostUdaju
n9:S
n3:entitaPredkladatele
n16:predkladatel
n3:idSjednocenehoVysledku
79493
n3:idVysledku
RIV/00216208:11110/13:10188753
n3:jazykVysledku
n18:eng
n3:klicovaSlova
Hypoxia-inducible factor 1 alpha; Heart defect; Diabetic embryopathy
n3:klicoveSlovo
n7:Diabetic%20embryopathy n7:Heart%20defect n7:Hypoxia-inducible%20factor%201%20alpha
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[325661172262]
n3:nazevZdroje
Journal of Molecular and Cellular Cardiology
n3:obor
n10:FA
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
5
n3:projekt
n6:GA301%2F09%2F0117 n6:GAP302%2F11%2F1308
n3:rokUplatneniVysledku
n21:2013
n3:svazekPeriodika
60
n3:tvurceVysledku
Bohuslavová, Romana Sedmera, David Škvorová, Lada Pavlínková, Gabriela Semenza, Gregg L.
n3:wos
000320429100017
n3:zamer
n14:AV0Z50520701
s:issn
0022-2828
s:numberOfPages
13
n22:doi
10.1016/j.yjmcc.2013.04.015
n4:organizacniJednotka
11110