Effects of maternal vitamin A status on fetal heart and  lung: changes in expression of key developmental genes

Antipatis, Christos; Ashworth, Cheryl; Grant, George; Lea, Richard G.; Hay, Susan M.; Rees, William D.

doi:10.1152/ajplung.1998.275.6.l1184

Cited by 34 publications

(33 citation statements)

References 17 publications

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“…Rat embryos which are deprived at later stages have an underdeveloped hindbrain, loss of posterior cranial nerves and posterior branchial arches, microphthalmia, narrow limb buds, neural crest cell death, failure or hypoplasia of lung development, failure of septation of the trachea and oesophagus, and lack of differentiation of neuronal populations in the brain (Dickman et al 1997;Antipatis et al 1998;White et al 1998). These studies have confirmed the role that RA plays in many systems of the embryo and at many times throughout development rather than at any one stage of development.…”

Section: Deprivation Studiesmentioning

confidence: 99%

The role of retinoic acid in embryonic and post-embryonic development

Maden

2000

Proc. Nutr. Soc.

116

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Retinoic acid (RA) is the bioactive metabolite of vitamin A (retinol) which acts on cells to establish or change the pattern of gene activity. Retinol is converted to RA by the action of two types of enzyme, retinol dehydrogenases and retinal dehydrogenases. In the nucleus RA acts as a ligand to activate two families of transcription factors, the RA receptors (RAR) and the retinoid X receptors (RXR) which heterodimerize and bind to the upstream sequences of RA-responsive genes. Thus, in addition to the well-established experimental paradigm of depriving animals of vitamin A to determine the role of RA in embryonic and post-embryonic development, molecular biology has provided us with two additional methodologies: knockout the enzymes or the RAR and RXR in the mouse embryo. The distribution of the enzymes and receptors, and recent experiments to determine the endogenous distribution of RA in the embryo are described here, as well as the effects on the embryo of knocking out the enzymes and receptors. In addition, recent studies using the classical vitamin A-deprivation technique are described, as they have provided novel insights into the regions of the embryo which crucially require RA, and the gene pathways involved in their development. Finally, the post-embryonic or regenerating systems in which RA plays a part are described, i.e. the regenerating limb, lung regeneration, hair cell regeneration in the ear and spinal cord regeneration in the adult.

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Section: Deprivation Studiesmentioning

confidence: 99%

The role of retinoic acid in embryonic and post-embryonic development

Maden

2000

Proc. Nutr. Soc.

116

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“…Several studies have shown the importance of vitamin A for proper lung morphogenesis and respiratory epithelium differentiation [Wilson et al, 1953;Antipatis et al, 1998;Morriss-Kay and Ward, 1999;Barlier-Mur et al, 2003;Perrotta et al, 2003]. Vitamin A deficiency was found to perturb lung branching morphogenesis and to alter the expression of pattern-related genes [Chailley-Heu et al, 1999].…”

Section: Discussionmentioning

confidence: 99%

Vitamin A deficiency in an infant with PAGOD syndrome

Gavrilova

Babovic

Lteif

et al. 2009

American J of Med Genetics Pt A

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PAGOD syndrome is a rare condition characterized by multiple congenital anomalies including pulmonary artery and lung hypoplasia, agonadism, diaphragmatic abnormalities, cardiac defects, omphalocele, and various genital anomalies. The etiology of this condition is unknown but the spectrum of birth defects is similar to the developmental anomalies observed in vitamin A deficiency animal models. We describe an infant with PAGOD syndrome phenotype. The patient had a normal male karyotype and no copy number changes were seen on chromosome genomic hybridization (CGH) microarray. Endocrine evaluation was consistent with primary hypogonadism. The testes and Müllerian structures were absent by imaging studies, raising the possibility of arrest of early gonadogenesis. The plasma free vitamin A was low, consistent with moderate to severe vitamin A deficiency; the maternal plasma vitamin A level was normal. During pregnancy maternal vitamin A is taken up by retinol binding protein 4 (RBP4) which is expressed in the embryonic visceral endoderm from pregastrulational stages. This transport is mediated via the specific membrane receptor for RBP, stimulated by retinoic acid 6 (STRA6). STRA6 is widely expressed in human organ systems including the placenta during embryonic development. Mutations in the STRA6 gene result in Matthew-Wood syndrome, which demonstrates significant phenotypic overlap with PAGOD syndrome. Sequencing of STRA6 coding regions in our patient, revealed no mutations. We present a case of PAGOD syndrome with a review of the literature, posing the hypothesis that a vitamin A metabolic defect, other than transport mediated by STRA6 receptor, might have an etiological role in the development of this multiple congenital anomalies syndrome.

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“…Our results show that maternal MVAD decreased body weight and lung weight of the newborn, but body weight showed no difference compared to the control at 8 wk of age. Other researches also have established that maternal VAD in the rat has marked effects on the fetus and neonate including impaired fetal lung development (13,14,32). It indicated that MVAD affects fetal and early postnatal lung viability, and can last to adulthood.…”

Section: Mvad From Prenatal Stage Reduces Body Weight and Lung Weightmentioning

confidence: 99%

Marginal Vitamin A Deficiency Affects Lung Maturation in Rats from Prenatal to Adult Stage

Wei

Huang

et al. 2009

J Nutr Sci Vitaminol

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Summary Mild or marginal vitamin A deficiency (MVAD) is still a serious and widespread public health problem in pregnant women and children in developing countries. This study investigated rat lung maturation from prenatal to adult stage during pregnancy and postnatal MVAD and the recovery after postnatal vitamin A supplementation (VAS). Adult female rats and their offspring were randomized into three groups. 1. Control: the mothers and offspring received a normal diet.2. MVAD: The mothers and offspring received a MVAD diet.3. VAS: the mothers received MVAD diet till parturition, and then received the normal diet. The offspring of the VAS group were given low-dose vitamin A from postnatal day 1 to day 7 and received the normal diet after weaning. The lung development, structure, and collagen and elastic fiber of offspring were monitored by morphometric analysis at age 1 d, 2 and 8 wk, respectively. Lower body weight, lung weight, reduced numbers of alveoli and total alveolar surface area as well as increased alveoli septa thickness was observed in MVAD compared to that in the control animals. Increased collagen deposits and decreasing elastic fiber were found in MVAD rats. However, all of these were significantly improved in VAS-treated animals. These data suggest that the rat lung is sensitive to MVAD during the developing stage. Early postnatal vitamin A supplementation can partially restore the normal lung structure.

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Effects of maternal vitamin A status on fetal heart and lung: changes in expression of key developmental genes

Cited by 34 publications

References 17 publications

The role of retinoic acid in embryonic and post-embryonic development

The role of retinoic acid in embryonic and post-embryonic development

Vitamin A deficiency in an infant with PAGOD syndrome

Marginal Vitamin A Deficiency Affects Lung Maturation in Rats from Prenatal to Adult Stage

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