Persistence of oligodendrocyte precursor cells and altered myelination in optic nerve associated to retina degeneration in mice devoid of all thyroid hormone receptors
Persistence of oligodendrocyte precursor cells and altered myelination in optic nerve associated to retina degeneration in mice devoid of all thyroid hormone receptors
复制标题
DOI：
10.1073/pnas.052482299
复制
发表时间：
2002-03-05
影响因子：
11.1
通讯作者：
Flamant, F
中科院分区：
文献类型：
--
作者：
Baas, D;Legrand, C;Flamant, F
甲状腺激素（3,5,3'-三碘-L-甲状腺氨酸或 T3）在中枢神经系统发育过程中发挥多效性活性。胎儿期和产后的甲状腺功能减退症会导致不可逆的智力低下综合征。在细胞水平上，T3 已知作用于神经元和神经胶质谱系并控制细胞增殖、凋亡、迁移和分化。出生时在视神经中发现的少突胶质细胞前体细胞 (OPC) 是自我更新细胞，通常在啮齿动物出生后的前 3 周内分化为有丝分裂后髓鞘形成少突胶质细胞。在体外，将 T3 添加到 OPC 中足以触发它们的终末分化。目前对 T3 受体敲除小鼠的分析表明，所有 T3 受体的缺失会导致成年视神经中 OPC 持续增殖、髓鞘形成缺陷，有时还会导致视网膜神经节神经元退化。因此，T3信号传导对于体外促进OPC的完全分化是必要的。
Thyroid hormone (3,5,3'-triiodo-L-thyronine or T3) exerts a pleiotropic activity during central nervous system development. Hypothyroidism during the fetal and postnatal life results in an irreversible mental retardation syndrome. At the cellular level, T3 is known to act on neuronal and glial lineages and to control cell proliferation, apoptosis, migration, and differentiation. oligodendrocyte precursor cells (OPC) found at birth in the optic nerves are self-renewing cells that normally differentiate during the first 3 weeks of rodent postnatal life into postmitotic myelinating oligoclendrocytes. In vitro, the addition of T3 to OPC is sufficient to trigger their terminal differentiation. The present analysis of T3 receptor knockout mice reveals that the absence of all T3 receptor results in the persistence of OPC proliferation in adult optic nerves, in a default in myelination, and sometimes in the degeneration of the retinal ganglion neurons. Thus, T3 signaling is necessary in vitro to promote the complete differentiation of OPC.