Vitamin A and embryonic development: an overview.

Vitamin A and embryonic development: an overview.
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维生素 A 和胚胎发育:概述。

DOI:
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发表时间:
1998
期刊:
Journal of NutriLife
影响因子:
--
通讯作者:
M. Zile
M. Zile
中科院分区:
--
文献类型:
--
作者:
M. Zile

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维生素A是整个生命周期必需的微量营养素。其活性形式,即通过类视黄醇受体产生的视黄酸,参与调节发育的信号转导途径。胚胎发育过程中维生素A的缺乏和过量都会导致先天畸形。检查维生素 A 在胚胎发育中的功能的方法包括用过量的类维生素A治疗和使用类维生素A受体敲除小鼠,这为了解类维生素A信号系统的复杂性提供了重要的见解。最近探索的一个模型是类维生素A配体敲除,即维生素A缺乏的胚胎。可以在缺乏维生素 A 的禽类胚胎中成功检查早期发育,其中生物活性类视黄醇可以挽救缺陷的基因型和表型。在该模型中,可以明确地将维生素 A 的生理功能与心脏、胚胎循环和中枢神经系统的发育以及心脏不对称的调节联系起来。已鉴定出早期胚胎发生过程中受内源维生素 A 调节的几种发育基因。类维生素A受体及其内源性配体(维生素A活性形式)存在于早期胚胎中。维生素 A 活性形式通过不同的时空代谢途径进行发育调节的生物生成,与胚胎发育过程中类视黄醇信号转导的启动至关重要。
Vitamin A is an essential micronutrient throughout the life cycle. Its active form, retinoic acid via retinoid receptors, is involved in signal transduction pathways regulating development. Both the lack and excess of vitamin A during embryonic development result in congenital malformations. Approaches to examine the function of vitamin A in embryonic development have included treatment with excess retinoids and the use of retinoid receptor knock-out mice, which have provided important insights into the complexity of the retinoid signaling system. A recently explored model is the retinoid ligand knock-out, i.e., the vitamin A-deficient embryo. Early development can be successfully examined in the vitamin A-deficient avian embryo, in which bioactive retinoids can rescue the deficient genotype as well as phenotype. In this model it has been possible to unequivocally link the physiological function of vitamin A to development of heart, embryonal circulatory and central nervous systems and the regulation of heart asymmetry. Several developmental genes regulated by endogenous vitamin A during early embryogenesis have been identified. Retinoid receptors and their endogenous ligands, the vitamin A-active forms, are present in the early embryo. It is the developmentally regulated biogeneration of the vitamin A-active forms via distinct spatio-temporal metabolic pathways that is critically linked to the initiation of retinoid signal transduction during embryonic development.
来自缺乏维生素 A 的鹌鹑胚胎的 Hensen 节诱导雏鸡肢芽复制,并保留其正常的 Sonic Hedgehog (Shh) 不对称表达。
DOI: 10.1006/dbio.1996.0021
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影响因子: --
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DOI: 10.1006/dbio.1996.0005
发表时间: 1996
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影响因子: --
作者:
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