Suppression of retinoic acid receptors may contribute to embryonic skeleton hypoplasia in maternal rats with chronic vitamin A deficiency

Li, Na; Sun, Shanshan; Wang, Di; Yao, Ping; Yang, Xuefeng; Yan, Hong; Du, Yukai; Ying, Chengjiang; Liu, Liegang

doi:10.1016/j.jnutbio.2009.04.011

Cited by 10 publications

(8 citation statements)

References 46 publications

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“…Our findings support the hypothesis that maternal VAD could induce vertebral anomalies in the offspring. Our study has also observed other skeletal abnormalities include loss of the neural arch of cervical vertebrae 1, malformation of sternum, loss of the ribs, rib fusion, abnormal of forelimb and hindlimb, malformation of the pelvic regions, which have also been observed by others [24,30]. Another important finding of our study is that VAD repressed the expression RALDHs and RARs, which are important components of RA signaling, in the liver and vertebral body of VAD rats.…”

Section: Discussionsupporting

confidence: 88%

Vitamin A Deficiency Induces Congenital Spinal Deformities in Rats

Shen

2013

The Spine Journal

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Section: Discussionsupporting

confidence: 88%

Vitamin A Deficiency Induces Congenital Spinal Deformities in Rats

Shen

2013

The Spine Journal

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“…In our study, which we designed to examine a narrower physiological range of VA intake that is representative of most human diets, we observed a reduction in limb size (femur length) in neonates from VAM dams, whereas obvious severe dysostosis was not observed. This may be due to the fact that our VAM diet was not extremely low in VA, ;5 times more than that used by Li et al (28). Moreover, the HZ of femur chondrocytes was significantly shorter in pups from VAM dams, and only in the VAM group did oral feeding with VARA significantly increase the length of the HZ.…”

Section: Resultsmentioning

confidence: 76%

“…Li et al (28) reported that VA deficiency caused embryonic skeleton hypoplasia, including retardation of ossification and reduction in the size of the skeleton, and limb dysostosis. In our study, which we designed to examine a narrower physiological range of VA intake that is representative of most human diets, we observed a reduction in limb size (femur length) in neonates from VAM dams, whereas obvious severe dysostosis was not observed.…”

Section: Resultsmentioning

confidence: 99%

Perinatal Exposure to Vitamin A Differentially Regulates Chondrocyte Growth and the Expression of Aggrecan and Matrix Metalloprotein Genes in the Femur of Neonatal Rats

Zhang

Wray

Ross

2012

The Journal of Nutrition

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Vitamin A (VA) and its active form, retinoic acid (RA), are regulators of skeletal development. In the present study, we investigated if maternal VA intake during pregnancy and lactation, as well as direct oral supplementation of neonates with VA + RA (VARA) in early life, alters neonatal bone formation and chondrocyte gene expression. Offspring of dams fed 3 levels of VA (marginal, adequate, and supplemented) for 10 wk were studied at birth (P0) and postnatal day 7 (P7). One-half of the newborns received an oral supplement of VARA on P1, P4, and P7. Tissues were collected on P0 and 6 h after the last dose on P7. Pup plasma and liver retinol concentrations were increased by both maternal VA intake and VARA (P < 0.01). Although maternal VA did not affect bone mineralization as assessed by von Kossa staining, newborn femur length was increased with maternal VA (P < 0.05). VARA supplementation of neonates increased the length of the hypertrophic zone only in VA-marginal pups, close to that in neonates from VA-adequate dams, suggesting VARA caused a catching up of growth that was limited by low maternal VA intake. Maternal diet did not alter type X nor type II collagen mRNA. However, VARA-treated pups from VA-supplemented dams had reduced mRNA for aggrecan, a major component of cartilage matrix, and increased mRNA for matrix metalloproteinase (MMP)13, which catalyzes the degradation of aggrecan and collagens. These results suggest that moderately high maternal VA intake combined with neonatal VARA supplementation can reduce the ratio of aggrecan:MMP, which may unfavorably alter early bone development.

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“…Suppression of RAR receptors is involved in embryonic skeleton hypoplasia in embryos of vitamin A-deficient rats. 15 During embryonic development, RA is required for generating the correct anatomy of the spinal cord . Resveratrol improves diabetes-induced reduction in embryonic extracellular signal-regulated kinases (ERK1/2).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Prevents Impairment in Activation of Retinoic Acid Receptors and MAP Kinases in the Embryos of a Rodent Model of Diabetic Embryopathy

et al. 2012

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Diabetes induces impairments in gene expression during embryonic development that leads to premature and improper tissue specialization. Retinoic acid receptors (RARs and retinoid X receptor [RXRs]) and mitogen-activated protein kinases (MAPKs) play crucial roles during embryonic development, and their suppression or activation has been shown as a determinant of the fate of embryonic organogenesis. We studied the activation of RARs and MAPKs in embryonic day 12 (E12) in embryos of rats under normal, diabetic, and diabetic treated with resveratrol ([RSV]; 100 mg/kg body weight) conditions. We found downregulation of RARs and RXRs expressions as well as their DNA-binding activities in the embryos exhibiting developmental delays due to diabetes. Furthermore, the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 was decreased and phosphorylation of c-Jun N-terminal kinase (JNK) 1/2 and p38 was increased. Interestingly, embryos of diabetic rats treated with RSV showed normalized patterns of RARs, RXRs, neuronal markers, and ERK, JNK and p38 phosphorylation.

show abstract

Suppression of retinoic acid receptors may contribute to embryonic skeleton hypoplasia in maternal rats with chronic vitamin A deficiency

Cited by 10 publications

References 46 publications

Vitamin A Deficiency Induces Congenital Spinal Deformities in Rats

Vitamin A Deficiency Induces Congenital Spinal Deformities in Rats

Perinatal Exposure to Vitamin A Differentially Regulates Chondrocyte Growth and the Expression of Aggrecan and Matrix Metalloprotein Genes in the Femur of Neonatal Rats

Resveratrol Prevents Impairment in Activation of Retinoic Acid Receptors and MAP Kinases in the Embryos of a Rodent Model of Diabetic Embryopathy

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