| Vitamin A plays an important role in the growth and development of animals, which mainly generated by in vivo metabolite retinoic acid, especially in the embryonic stage of development. The regulation effects of Vitamin A on the development of the spine mainly by regulating the expression of Hox genes. Both of exogenous RA intervention or endogenous RA inactivation can also lead to abnormal Hox gene expression. Decreased levels of vitamin A pregnant mother can affect the growth and development of the offspring, which often leads to deformities Spinal deformities, including the craniovertebral junction de-formity. Studies have shown that Hox gene family gene-Hoxd3is the most important regulative gene in development of craniovertebral junction, and its lack of expression often induce craniovertebral junction deformity. However, vitamin A deficiency affecting normal embryonic development process is very complex, there are other regulatory mechanisms. Modern medical studies have shown that vitamin A and transforming growth factor-β has a close relationship during embryonic development, for the development of various tissues and organs of suppression or synergy with each other. TGF-β is a family of polypeptides with multiple functions, widely present in normal cells and transformed animal cells, which is most rich in the platelets and bone structure. TGF-β1as the significant member of the TGF-βs family, promote cell proliferation, cell differentiation, and extracellular matrix synthesis. More importantly, it could promote growth and differentiation of mesenchymal cells. therefore Vitamin A deficiency may lead to decreased TGF-β1expression in fetal, resulting in decrease in osteoblast differentiation, growth retardation of skeleton, craniovertebral junction deformities, and congenital skeleton mal-forma-tions.Objective:This paper is divided into literature review and experimental study in two parts. Literature review describes the interaction between the main role of vitamin A in embryonic development and the interaction with TGF-β and the regulation of Hox gene expression. Also it explains the mechanism of Hox gene that causes spinal deformity. Experimental study focused on vitamin A deficiency leads to reduced gene expression Hoxd3mechanism causing crani-overtebral junction deformities, and a lack of vitamin A in the process leading to craniovertebral junction deformities with TGF-β1possible correlation.Methods:36female C57BL/6mice were divided into2groups, namely normal control group (N), vitamin A deficiency group(VAD). N group were fed with normal diet, while VAD group were fed with vitamin A deficiency diet. After modeling success, half of mice had been cesareans and its embryos were taken for detecting the expression levels of Hoxd3gene AND retinoic acid receptors mRNA by RT-QPCR On11.5st gestational day. The rest of pregnant mice had been cesareans and its embryos were taken for detecting the level of TGF-β1by immunohistochemistry On21st gestational day.Result:(1)The expression levels of Hoxd3gene and RARs mRNA and were significantly lower in VAD group than N group (P<0.01).(2) There was significant difference in TGF-β1between N group and VAD group in craniovertebral junction (P<0.01).Conclusion:Vitamin A deficiency could decrease the expression level of Hoxd3gene related to depression of RARs during embryo development, which could induce congenital malformations of the craniovertebral junction. And we also found that Vitamin A deficiency could decrease the expression level of TGF-β1in bone mass of raniovertebral junction, which might indicate that the interaction between Vitamin A and TGF-β1in pattern of craniovertebral junction. |
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