Literature DB >> 15578651

Disturbed morphogenesis of cardiac outflow tract and increased rate of aortic arch anomalies in the offspring of diabetic rats.

Daniël G M Molin1, Pauline A M Roest, Hanna Nordstrand, Lambertus J Wisse, Robert E Poelmann, Ulf J Eriksson, Adriana C Gittenberger-De Groot.   

Abstract

BACKGROUND: Maternal diabetes (MD) is a risk factor for offspring to develop cardiovascular anomalies; this is of growing clinical concern since the number of women in childbearing age with compromised glucose homeostasis is increasing. Hyperglycemia abrogates cardiovascular development in vitro; however, a link to cardiovascular defects in diabetic offspring remains to be investigated.
METHODS: We have studied cardiovascular development in offspring of MD rats by examining serial histological sections of GD 12.0-18.0 offspring. Development of pharyngeal arch artery malformations was analyzed and related to intracardiac anomalies.
RESULTS: Pharyngeal arch artery and intracardiac defects were present in 27 of 37 MD GD 13.0-18.0 offspring. Early sixth arch arteries showed abrogated arteriogenesis, whereas fourth arch artery defects developed as a result of abnormal remodeling. Morphometrical analysis showed increased apoptosis in regressing artery segments and reduced apoptosis in persisting artery segments. Double outlet right ventricle with infundibular stenosis (tetralogy of Fallot) was predominantly found in combination with sixth artery defects and pulmonary atresia. As confirmed by morphometric analysis and three-dimensional (3D)-reconstructions, outflow tract defects coincided with endocardial cushion hypoplasia. Cases with teratology of Fallot additionally showed a shorter outflow tract. No relation with apoptosis or disturbed neural crest cell migration was found.
CONCLUSIONS: Our data uniquely demonstrate mechanistic differences involved in the development of sixth and fourth artery anomalies. Whereas increased apoptosis induces fourth artery anomalies, pulmonary outflow obstruction abrogates sixth artery differentiation independent of apoptosis. The model presented allows analysis of diabetic conditions on cardiovascular development in vivo, essential for elucidating this teratology.

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Year:  2004        PMID: 15578651     DOI: 10.1002/bdra.20101

Source DB:  PubMed          Journal:  Birth Defects Res A Clin Mol Teratol        ISSN: 1542-0752


  21 in total

1.  ASK1 mediates the teratogenicity of diabetes in the developing heart by inducing ER stress and inhibiting critical factors essential for cardiac development.

Authors:  Fang Wang; Yanqing Wu; Michael J Quon; Xuezheng Li; Peixin Yang
Journal:  Am J Physiol Endocrinol Metab       Date:  2015-07-14       Impact factor: 4.310

2.  TGFβ and Wnt in cardiac outflow tract defects in offspring of diabetic pregnancies.

Authors:  Zhiyong Zhao
Journal:  Birth Defects Res B Dev Reprod Toxicol       Date:  2014-09-17

3.  Oxidative stress during diabetic pregnancy disrupts cardiac neural crest migration and causes outflow tract defects.

Authors:  Sarah C Morgan; Frédéric Relaix; Lisa L Sandell; Mary R Loeken
Journal:  Birth Defects Res A Clin Mol Teratol       Date:  2008-06

4.  Superoxide Dismutase 1 In Vivo Ameliorates Maternal Diabetes Mellitus-Induced Apoptosis and Heart Defects Through Restoration of Impaired Wnt Signaling.

Authors:  Fang Wang; Steven A Fisher; Jianxiang Zhong; Yanqing Wu; Peixin Yang
Journal:  Circ Cardiovasc Genet       Date:  2015-07-31

5.  Type 2 diabetes mellitus induces congenital heart defects in murine embryos by increasing oxidative stress, endoplasmic reticulum stress, and apoptosis.

Authors:  Yanqing Wu; E Albert Reece; Jianxiang Zhong; Daoyin Dong; Wei-Bin Shen; Christopher R Harman; Peixin Yang
Journal:  Am J Obstet Gynecol       Date:  2016-03-31       Impact factor: 8.661

Review 6.  Diabetes and apoptosis: neural crest cells and neural tube.

Authors:  James H Chappell; Xiao Dan Wang; Mary R Loeken
Journal:  Apoptosis       Date:  2009-12       Impact factor: 4.677

7.  Cardiac function in 7-8-year-old offspring of women with type 1 diabetes.

Authors:  Maarten Rijpert; Johannes M P J Breur; Inge M Evers; Harold W de Valk; Cobi J Heijnen; Folkert J Meijboom; Gerard H A Visser
Journal:  Exp Diabetes Res       Date:  2011-11-15

8.  Hyperglycemia slows embryonic growth and suppresses cell cycle via cyclin D1 and p21.

Authors:  Devon E Scott-Drechsel; Sandra Rugonyi; Daniel L Marks; Kent L Thornburg; Monica T Hinds
Journal:  Diabetes       Date:  2012-11-27       Impact factor: 9.461

9.  Specific local cardiovascular changes of Nepsilon-(carboxymethyl)lysine, vascular endothelial growth factor, and Smad2 in the developing embryos coincide with maternal diabetes-induced congenital heart defects.

Authors:  Pauline A M Roest; Daniël G M Molin; Casper G Schalkwijk; Liesbeth van Iperen; Parri Wentzel; Ulf J Eriksson; Adriana C Gittenberger-de Groot
Journal:  Diabetes       Date:  2009-02-02       Impact factor: 9.461

10.  Maternal diabetes induces congenital heart defects in mice by altering the expression of genes involved in cardiovascular development.

Authors:  Srinivasan Dinesh Kumar; S Thameem Dheen; Samuel Sam Wah Tay
Journal:  Cardiovasc Diabetol       Date:  2007-10-30       Impact factor: 9.951

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