Thyroid hormone action: astrocyte-neuron communication.
Thyroid hormone action: astrocyte-neuron communication.
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DOI：
10.3389/fendo.2014.00082
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发表时间：
2014
影响因子：
5.2
通讯作者：
Bernal J
中科院分区：
文献类型：
--
作者：
Morte B;Bernal J
甲状腺激素 (TH) 的作用主要是通过 T3 与核受体结合来调节基因表达来发挥作用。 T4 通过星形胶质细胞中表达的 2 型脱碘酶 (D2) 的作用，作为中枢神经系统细胞内 T3 的来源发挥着重要作用。神经细胞 T3 可用性模型已被提出并验证。该模型认为大脑 T3 具有双重来源：一部分可直接从循环中获得，另一部分则由星形胶质细胞中的 T4 通过 D2 局部产生。胎儿大脑几乎完全依赖于本地产生的T3。全身 T3 的贡献随后在发育过程中增加，在产后后期和成年阶段约占大脑总 T3 的 50%。在本文中，我们回顾了支持该模型的实验数据，以及影响大脑中 T3 可用性的因素（例如脱碘酶和转运蛋白）如何在发育过程中调节局部 TH 作用中发挥决定性作用。
Thyroid hormone (TH) action is exerted mainly through regulation of gene expression by binding of T3 to the nuclear receptors. T4 plays an important role as a source of intracellular T3 in the central nervous system via the action of the type 2 deiodinase (D2), expressed in the astrocytes. A model of T3 availability to neural cells has been proposed and validated. The model contemplates that brain T3 has a double origin: a fraction is available directly from the circulation, and another is produced locally from T4 in the astrocytes by D2. The fetal brain depends almost entirely on the T3 generated locally. The contribution of systemic T3 increases subsequently during development to account for approximately 50% of total brain T3 in the late postnatal and adult stages. In this article, we review the experimental data in support of this model, and how the factors affecting T3 availability in the brain, such as deiodinases and transporters, play a decisive role in modulating local TH action during development.
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