Vitamin A deficiency induces congenital spinal deformities in rats.

Most cases of congenital spinal deformities were sporadic and without strong evidence of heritability. The etiology of congenital spinal deformities is still elusive and assumed to be multi-factorial. The current study seeks to elucidate the effect of maternal vitamin A deficiency and the production...

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Main Authors: Zheng Li, Jianxiong Shen, William Ka Kei Wu, Xiaojuan Wang, Jinqian Liang, Guixing Qiu, Jiaming Liu
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3465343?pdf=render
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spelling doaj-3f875de13ef54b11865ed24e099fbd5c2020-11-25T01:22:44ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-01710e4656510.1371/journal.pone.0046565Vitamin A deficiency induces congenital spinal deformities in rats.Zheng LiJianxiong ShenWilliam Ka Kei WuXiaojuan WangJinqian LiangGuixing QiuJiaming LiuMost cases of congenital spinal deformities were sporadic and without strong evidence of heritability. The etiology of congenital spinal deformities is still elusive and assumed to be multi-factorial. The current study seeks to elucidate the effect of maternal vitamin A deficiency and the production of congenital spinal deformities in the offsping. Thirty two female rats were randomized into two groups: control group, which was fed a normal diet; vitamin A deficient group, which were given vitamin A-deficient diet from at least 2 weeks before mating till delivery. Three random neonatal rats from each group were killed the next day of parturition. Female rats were fed an AIN-93G diet sufficient in vitamin A to feed the rest of neonates for two weeks until euthanasia. Serum levels of vitamin A were assessed in the adult and filial rats. Anteroposterior (AP) spine radiographs were obtained at week 2 after delivery to evaluate the presence of the skeletal abnormalities especially of spinal deformities. Liver and vertebral body expression of retinaldehyde dehydrogenase (RALDHs) and RARs mRNA was assessed by reverse transcription-real time PCR. VAD neonates displayed many skeletal malformations in the cervical, thoracic, the pelvic and sacral and limbs regions. The incidence of congenital scoliosis was 13.79% (8/58) in the filial rats of vitamin A deficiency group and 0% in the control group. Furthermore, vitamin A deficiency negatively regulate the liver and verterbral body mRNA levels of RALDH1, RALDH2, RALDH3, RAR-α, RAR-β and RAR-γ. Vitamin A deficiency in pregnancy may induce congenital spinal deformities in the postnatal rats. The decreases of RALDHs and RARs mRNA expression induced by vitamin A deprivation suggest that vertebral birth defects may be caused by a defect in RA signaling pathway during somitogenesis.http://europepmc.org/articles/PMC3465343?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Zheng Li
Jianxiong Shen
William Ka Kei Wu
Xiaojuan Wang
Jinqian Liang
Guixing Qiu
Jiaming Liu
spellingShingle Zheng Li
Jianxiong Shen
William Ka Kei Wu
Xiaojuan Wang
Jinqian Liang
Guixing Qiu
Jiaming Liu
Vitamin A deficiency induces congenital spinal deformities in rats.
PLoS ONE
author_facet Zheng Li
Jianxiong Shen
William Ka Kei Wu
Xiaojuan Wang
Jinqian Liang
Guixing Qiu
Jiaming Liu
author_sort Zheng Li
title Vitamin A deficiency induces congenital spinal deformities in rats.
title_short Vitamin A deficiency induces congenital spinal deformities in rats.
title_full Vitamin A deficiency induces congenital spinal deformities in rats.
title_fullStr Vitamin A deficiency induces congenital spinal deformities in rats.
title_full_unstemmed Vitamin A deficiency induces congenital spinal deformities in rats.
title_sort vitamin a deficiency induces congenital spinal deformities in rats.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2012-01-01
description Most cases of congenital spinal deformities were sporadic and without strong evidence of heritability. The etiology of congenital spinal deformities is still elusive and assumed to be multi-factorial. The current study seeks to elucidate the effect of maternal vitamin A deficiency and the production of congenital spinal deformities in the offsping. Thirty two female rats were randomized into two groups: control group, which was fed a normal diet; vitamin A deficient group, which were given vitamin A-deficient diet from at least 2 weeks before mating till delivery. Three random neonatal rats from each group were killed the next day of parturition. Female rats were fed an AIN-93G diet sufficient in vitamin A to feed the rest of neonates for two weeks until euthanasia. Serum levels of vitamin A were assessed in the adult and filial rats. Anteroposterior (AP) spine radiographs were obtained at week 2 after delivery to evaluate the presence of the skeletal abnormalities especially of spinal deformities. Liver and vertebral body expression of retinaldehyde dehydrogenase (RALDHs) and RARs mRNA was assessed by reverse transcription-real time PCR. VAD neonates displayed many skeletal malformations in the cervical, thoracic, the pelvic and sacral and limbs regions. The incidence of congenital scoliosis was 13.79% (8/58) in the filial rats of vitamin A deficiency group and 0% in the control group. Furthermore, vitamin A deficiency negatively regulate the liver and verterbral body mRNA levels of RALDH1, RALDH2, RALDH3, RAR-α, RAR-β and RAR-γ. Vitamin A deficiency in pregnancy may induce congenital spinal deformities in the postnatal rats. The decreases of RALDHs and RARs mRNA expression induced by vitamin A deprivation suggest that vertebral birth defects may be caused by a defect in RA signaling pathway during somitogenesis.
url http://europepmc.org/articles/PMC3465343?pdf=render
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