IMMUNOFLUORESCENT LOCALIZATION OF THYROID-HORMONE RECEPTOR ISOFORMS IN GLIAL-CELLS OF RAT-BRAIN
IMMUNOFLUORESCENT LOCALIZATION OF THYROID-HORMONE RECEPTOR ISOFORMS IN GLIAL-CELLS OF RAT-BRAIN
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DOI：
10.1210/en.135.5.1831
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发表时间：
1994-11-01
期刊：
影响因子：
4.8
通讯作者：
OPPENHEIMER, JH
中科院分区：
文献类型：
--
作者：
CARLSON, DJ;STRAIT, KA;OPPENHEIMER, JH
目前已知的三种Tg结合甲状腺激素受体（TR）异构体，TR α 1， TR β 1和TR β 2，源于两个不同的基因（α和β），而两种密切相关的非t -3结合受体变体，统称为TR α 2，源于α基因转录物的交替剪接。使用一组针对这些亚型的特异性抗血清，我们评估了大鼠大脑和小脑的少突胶质细胞和星形胶质细胞中TRs的存在或缺失。受体同位异构体和细胞特异性标记蛋白的共定位是基于配对免疫荧光探针差异发射的免疫组织化学分析。髓鞘碱性蛋白（MBP）抗血清鉴定少突胶质细胞，胶质纤维酸性蛋白鉴定星形胶质细胞。mbp阳性少突胶质细胞对三种TR亚型特异性抗血清和受体变体的抗血清均显示阳性荧光信号。这些发现与MBP基因是甲状腺激素作用的直接靶点的概念是一致的。TR的免疫反应性似乎主要局限于这些细胞的细胞核。相反，我们在胶质纤维酸性蛋白阳性星形胶质细胞中没有观察到任何TR亚型的免疫荧光信号。这些发现提出了一种可能性，即甲状腺激素对星形胶质细胞功能和结构的任何影响都是通过甲状腺激素与位于非星形胶质细胞中的受体相互作用或非核机制间接介导的。
The three currently recognized Tg binding thyroid hormone receptor (TR) isoforms, TR alpha 1, TR beta 1, and TR beta 2, arise from two distinct genes (alpha and beta), whereas two closely related non-T-3-binding receptor variants, collectively designated TR alpha 2, arise from alternate splicing of the alpha gene transcript. Using a panel of specific antisera to these isoforms we have assessed the presence or absence of TRs in oligodendrocytes and astrocytes of rat cerebrum and cerebellum. Inferences as to colocalization of the receptor isoforms and cell-specific marker proteins were based on immunohistochemical analysis of the differential emissions of paired immunofluorescent probes. Antisera against myelin basic protein (MBP) identified oligodendroglia, and glial fibrillary acidic protein identified astrocytes. MBP-positive oligodendrocytes displayed positive fluorescent signals with each of the three TR isoform-specific antisera and the antiserum to the receptor variants. These findings are consistent with the concept that the MBP gene is a direct target for thyroid hormone action. TR immunoreactivity appeared to localize primarily to the nuclei of these cells. In contrast, we observed no immunofluorescent signals for any of the TR isoforms in glial fibrillary acidic protein-positive astrocytes. These findings raise the possibility that any effect of thyroid hormone on astrocyte function and structure is mediated indirectly as a result of interaction of thyroid hormone with receptors situated in nonastrocyte cells or as a result of nonnuclear mechanisms.