Modeling anterior development in mice: Diet as modulator of risk for neural tube defects

Kappen, Claudia

doi:10.1002/ajmg.c.31380

Cited by 18 publications

(17 citation statements)

References 236 publications

(367 reference statements)

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“…The ef--fects from maternal exposure to nitrosatable drugs, fertility treat--ments, and nutrition intake such as folic acid intake may lead to ep--igenetic changes that are distrib--uted unequally to developing twins in utero, potentially affect--ing dentofacial formation. Folic acid consumption for example af--fects neural tube closure, which in turn impacts brain and craniofacial structures later on in development [11].…”

Section: Resultsmentioning

confidence: 99%

Assessment of dentofacial variations in monozygotic twins

2017

d3000

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With dentofacial development being a mul4factorial process, we face the ques1on of whether gene#c or environ--mental factors play a larger role in specific phenotypic traits. The use of twin studies allows one to employ gene/c controls to the study such that one can focus solely on traits that may be more environmentally determined. This study involves retrospec0ve as well as current analy0cal measurements between a set of monozygo0c twins to assess gene$c and outside influences on facial and intraoral development. While similari$es were acknowledged, we found differences in measurements of the facial thirds, the congenital presence of mandibular third molars, and the pres--ence of mandibular tori.Cita%on: Tu, V. (2017) Assessment of dentofacial varia%ons in monozygo%c twins. Den$stry 3000.

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Section: Resultsmentioning

confidence: 99%

Assessment of dentofacial variations in monozygotic twins

2017

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“…Other nutrients have emerged from retrospective studies as potential factors to influence the incidence of NTDs (Scott et al, 1990;Czeizel, 2009;Czeizel and Banhidy, 2011;Kappen, 2013). Iron deficiency is one of the most common micronutrient deficiencies in women of childbearing age (Lopez et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

High levels of iron supplementation prevents neural tube defects in the Fpn1^ffe mouse model

Stokes

Sabatino

Zohn

2017

Birth Defects Research

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Background Periconception maternal nutrition and folate in particular are important factors influencing the incidence of Neural Tube Defects (NTDs). Many but not all NTDs are prevented by folic acid supplementation and there is a pressing need for additional strategies to prevent these birth defects. Other micronutrients such as iron are potential candidates, yet a clear role for iron deficiency in contributing to NTDs is lacking. Our previous studies with the flatiron (ffe) mouse model of Ferroportin1 (Fpn1) deficiency suggest that iron is required for neural tube closure and forebrain development raising the possibility that iron supplementation could prevent NTDs. Methods We determined the effect of periconception iron and/or folic acid supplementation on the penetrance of NTDs in the Fpn1ffe mouse model. Concurrently, measurements of folate and iron were made to ensure supplementation had the intended effects. Results High levels of iron supplementation significantly reduced the incidence of NTDs in Fpn1ffe mutants. Fpn1 deficiency resulted in reduced folate levels in both pregnant dams and embryos. Yet folic acid supplementation did not prevent NTDs in the Fpn1ffe model. Similarly, forebrain truncations were rescued with iron. Surprisingly, the high levels of iron supplementation used in this study caused folate deficiency in wildtype dams and embryos. Conclusions Our results demonstrate that iron supplementation can prevent NTDs and forebrain truncations in the Fpn1ffe model. Surprisingly, high levels of iron supplementation and iron overload can cause folate deficiency. If iron is essential for neural tube closure, it is possible that iron deficiency might contribute to NTDs.

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“…After closure 2 meets closure 1 at the midbrain/hindbrain neuropore, and closure 3 meets closure 2 at the anterior neuropore, the whole neural tube closes completely [1, 3]. With the contribution of genetic and environmental factors, neural tube may fail to close, causing neural tube defects (NTDs) [4]. NTDs are the second most common birth defects with an incidence of 1:1000 in human births, after congenital heart defects [3].…”

Section: Introductionmentioning

confidence: 99%

Lacking of palladin leads to multiple cellular events changes which contribute to NTD

et al. 2017

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BackgroundThe actin cytoskeleton-associated protein palladin plays an important role in cell motility, morphogenesis and adhesion. In mice, Palladin deficient embryos are lethal before embryonic day (E) 15.5, and exhibit severe cranial neural tube and body wall closure defects. However, the mechanism how palladin regulates the process of cranial neural tube closure (NTC) remains unknown.MethodsIn this paper, we use gene knockout mouse to elucidate the function of palladin in the regulation of NTC process.ResultsWe initially focuse on the expression pattern of palladin and found that in embryonic brain, palladin is predominantly expressed in the neural folds at E9.5. We further check the major cellular events in the neural epithelium that may contribute to NTC during the early embryogenesis. Palladin deficiency leads to a disturbance of cytoskeleton in the neural tube and the cultured neural progenitors. Furthermore, increased cell proliferation, decreased cell differentiation and diminished apical cell apoptosis of neural epithelium are found in palladin deficient embryos. Cell cycle of neural progenitors in Palladin -/- embryos is much shorter than that in wt ones. Cell adhesion shows a reduction in Palladin -/- neural tubes.Conclusions Palladin is expressed with proper spatio-temporal pattern in the neural folds. It plays a crucial role in regulating mouse cranial NTC by modulating cytoskeleton, proliferation, differentiation, apoptosis, and adhesion of neural epithelium. Our findings facilitate further study of the function of palladin and the underlying molecular mechanism involved in NTC.Electronic supplementary materialThe online version of this article (doi:10.1186/s13064-017-0081-6) contains supplementary material, which is available to authorized users.

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Modeling anterior development in mice: Diet as modulator of risk for neural tube defects

Cited by 18 publications

References 236 publications

Assessment of dentofacial variations in monozygotic twins

Assessment of dentofacial variations in monozygotic twins

High levels of iron supplementation prevents neural tube defects in the Fpn1^ffe mouse model

Lacking of palladin leads to multiple cellular events changes which contribute to NTD

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Modeling anterior development in mice: Diet as modulator of risk for neural tube defects

Cited by 18 publications

References 236 publications

Assessment of dentofacial variations in monozygotic twins

Assessment of dentofacial variations in monozygotic twins

High levels of iron supplementation prevents neural tube defects in the Fpn1ffe mouse model

Lacking of palladin leads to multiple cellular events changes which contribute to NTD

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High levels of iron supplementation prevents neural tube defects in the Fpn1^ffe mouse model