Zou L, Burmeister L A, Styren S D, Kochanek P M, DeKosky S T
Department of Psychiatry, University of Pittsburgh, Pennsylvania, USA.
J Neurochem. 1998 Aug;71(2):887-90. doi: 10.1046/j.1471-4159.1998.71020887.x.
Type 2 5'-deiodinase (5'-D2), which converts thyroxine to the more active thyroid hormone 3,5,3'-triiodothyronine (T3), is believed to be an important source of intracellular T3 in the brain. The activity of this enzyme is increased in hypothyroidism and decreased in hyperthyroidism, and as such, it serves an important role to protect the brain from wide fluctuations in T3 during changes in thyroidal state. Although it has been hypothesized that T3 may facilitate neuronal regeneration after CNS injury, the 5'-D2 response to brain injury is unknown. To assess the 5'-D2 mRNA response to injury, we performed in situ hybridization following traumatic brain injury. In unlesioned animals, 5'-D2 mRNA was undetectable. At 3 days posttrauma, 5'-D2 mRNA was detected in ipsilateral cortex near the contusion. A significant further increase of 5'-D2 mRNA was noted 7 days posttrauma in both hippocampus and cortex. Similar response was also observed on the contralateral side. Colocalization of 5'-D2 mRNA with glial fibrillary acidic protein indicates that reactive astrocytes were the major cellular source for the trauma-induced 5'-D2 expression. These data demonstrate, for the first time, a trauma-induced, astrocytic up-regulation of 5'-D2 mRNA, suggesting a potential role for T3 action in adult brain's response to injury and recovery.
2型5'-脱碘酶（5'-D2）可将甲状腺素转化为活性更强的甲状腺激素3,5,3'-三碘甲腺原氨酸（T3），被认为是大脑中细胞内T3的重要来源。该酶的活性在甲状腺功能减退时升高，在甲状腺功能亢进时降低，因此，它在保护大脑免受甲状腺状态变化期间T3的大幅波动方面发挥着重要作用。尽管有假说认为T3可能促进中枢神经系统损伤后神经元的再生，但5'-D2对脑损伤的反应尚不清楚。为了评估5'-D2 mRNA对损伤的反应，我们在创伤性脑损伤后进行了原位杂交。在未受伤的动物中，检测不到5'-D2 mRNA。创伤后3天，在挫伤附近的同侧皮质中检测到5'-D2 mRNA。创伤后7天，海马体和皮质中的5'-D2 mRNA均显著进一步增加。在对侧也观察到类似反应。5'-D2 mRNA与胶质纤维酸性蛋白的共定位表明，反应性星形胶质细胞是创伤诱导的5'-D2表达的主要细胞来源。这些数据首次证明了创伤诱导的星形胶质细胞5'-D2 mRNA上调，提示T3作用在成人大脑对损伤和恢复的反应中具有潜在作用。
