Thyroid hormone activates oligodendrocyte precursors and increases a myelin-forming protein and NGF content in the spinal cord during experimental allergic encephalomyelitis
Thyroid hormone activates oligodendrocyte precursors and increases a myelin-forming protein and NGF content in the spinal cord during experimental allergic encephalomyelitis
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DOI：
10.1073/pnas.052704499
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发表时间：
2002-03-05
影响因子：
11.1
通讯作者：
Giardino, L
中科院分区：
文献类型：
--
作者：
Calza, L;Fernandez, M;Giardino, L
在脱髓鞘疾病的不同实验模型中，已经证实了成人中枢神经系统的重新髓鞘形成。然而，没有明确的证据表明多发性硬化症会发生重新髓鞘形成，多发性硬化症是最弥漫的脱髓鞘疾病。在这篇文章中，我们探索了在实验性变态反应性脑脊髓炎中促进髓鞘形成的可能性，这是一种广泛使用的多发性硬化症的实验模型，方法是招募前体细胞，并通过给予甲状腺激素(T4)将其导入少突胶质细胞系。实验性变态反应性脑脊髓炎动物脑室下区和脊髓内大量增殖细胞(BrdUrd摄取和Ki67-IR)和未分化前体标记物(Nestin)表达增加。T4治疗降低了脊髓、嗅球和脑室下区少突胶质细胞前体细胞[多唾液酸化神经细胞黏附分子(PSA-NCAM)，O4，A2B5]和成熟少突胶质细胞(髓鞘碱性蛋白)的增殖和巢蛋白免疫反应，上调了少突胶质细胞前体[PSA-NCAM，O4，A2B5]和成熟少突胶质细胞(髓鞘碱性蛋白)的表达。
Remyelination in the adult central nervous system has been demonstrated in different experimental models of demyelinating diseases. However, there is no clear evidence that remyelination occurs in multiple sclerosis, the most diffuse demyelinating disease. In this article, we explore the possibility of promoting myelination in experimental allergic encephalomyelitis, a widely used experimental model of multiple sclerosis, by recruiting progenitors and channeling them into oligodendroglial lineage through administration of thyroid hormone (T4). A large number of proliferating cells (BrdUrd uptake and Ki67-IR) and the expression of markers for undifferentiated precursors (nestin) increased in the subventricular zone and spinal cord of experimental allergic encephalomyelitis animals. T4 administration reduces proliferation and nestin-immunoreactivity and up-regulates expression of markers for oligodendrocyte progenitors [polysialylated-neural cell adhesion molecule (PSA-NCAM), O4, A2B5] and mature oligodendrocytes (myelin basic protein) in the spinal cord, olfactory bulb, and subventricular zone.