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3,5,3'-triiodo-L-thyronine interacts with the genome by binding and activating nuclear 3,5,3'-triiodo-L-thyronine receptors. To determine how in secondary oligodendrocyte cultures, exogenous 3,5,3'-triiodo-L-thyronine influences the expression of different 3,5,3'-triiodo-L-thyronine receptor isoforms, we studied the regulation of alpha 1, alpha 2 and beta 1 3,5,3'-triiodo-L-thyronine receptor mRNAs. In culture, we find that beta 1, 3,5,3'-triiodo-L-thyronine receptor mRNA, but not alpha 1 and alpha 2 3,5,3'-triiodo-L-thyronine receptor mRNAs, is up-regulated by 3,5,3'-triiodo-L-thyronine in a time and dose dependent manner. In addition, we present evidence indicating that beta 1 3,5,3'-triiodo-L-thyronine receptor expression is posttranscriptionally regulated by 3,5,3'-triiodo-L-thyronine. Previous studies from our laboratory and others have shown that in the rat oligodendrocyte lineage, 3,5,3'-triiodo-L-thyronine receptors alpha 1 and alpha 2 were expressed in both early progenitor cells and mature oligodendrocytes. In contrast, beta 1 3,5,3'-triiodo-L-thyronine receptor was found to be expressed only in mature oligodendrocytes. This suggests that thyroid hormone may influence oligodendrocyte differentiation and maturation via 3,5,3'-triiodo-L-thyronine receptor beta 1, which is expressed only in oligodendrocytes and not in progenitor cells. We therefore show that this effect is indirect and is mediated by 3,5,3'-triiodo-L-thyronine which acts posttranscriptionally on the 3,5,3'-triiodo-L-thyronine receptor beta 1 gene.3,5,3'-triiodo-L-thyronine interacts with the genome by binding and activating nuclear 3,5,3'-triiodo-L-thyronine receptors. To determine how in secondary oligodendrocyte cultures, exogenous 3,5,3'-triiodo-L-thyronine influences the expression of different 3,5,3'-triiodo-L-thyronine receptor isoforms, we studied the regulation of alpha 1, alpha 2 and beta 1 3,5,3'-triiodo-L-thyronine receptor mRNAs. In culture, we find that beta 1, 3,5,3'-triiodo-L-thyronine receptor mRNA, but not alpha 1 and alpha 2 3,5,3'-triiodo-L-thyronine receptor mRNAs, is up-regulated by 3,5,3'-triiodo-L-thyronine in a time and dose dependent manner. In addition, we present evidence indicating that beta 1 3,5,3'-triiodo-L-thyronine receptor expression is posttranscriptionally regulated by 3,5,3'-triiodo-L-thyronine. Previous studies from our laboratory and others have shown that in the rat oligodendrocyte lineage, 3,5,3'-triiodo-L-thyronine receptors alpha 1 and alpha 2 were expressed in both early progenitor cells and mature oligodendrocytes. In contrast, beta 1 3,5,3'-triiodo-L-thyronine receptor was found to be expressed only in mature oligodendrocytes. This suggests that thyroid hormone may influence oligodendrocyte differentiation and maturation via 3,5,3'-triiodo-L-thyronine receptor beta 1, which is expressed only in oligodendrocytes and not in progenitor cells. We therefore show that this effect is indirect and is mediated by 3,5,3'-triiodo-L-thyronine which acts posttranscriptionally on the 3,5,3'-triiodo-L-thyronine receptor beta 1 gene.

To determine which thyroid receptor (TR) isoforms are expressed during oligodendrocyte differentiation, we studied the expression of the mRNAs encoding two alpha (alpha 1 and alpha 2) and one beta (beta 1) TR isoforms in a bipotential oligodendrocyte-type 2-astrocyte (O-2A) progenitor cell line (CG-4) as well as in rat O-2A progenitor cells and oligodendrocytes. O-2A progenitor cells expressed only TR alpha-mRNAs, whereas oligodendrocytes and type 2-astrocytes also expressed TR beta 1-mRNAs. The differential expression of alpha 1 and beta 1 TRs suggests specific functions for both types of TRs during oligodendrocyte differentiation. We present evidence for a possible role of TR alpha 1 in the effect of thyroid hormones on the proliferation of CG-4 cells maintained as progenitor cells.To determine which thyroid receptor (TR) isoforms are expressed during oligodendrocyte differentiation, we studied the expression of the mRNAs encoding two alpha (alpha 1 and alpha 2) and one beta (beta 1) TR isoforms in a bipotential oligodendrocyte-type 2-astrocyte (O-2A) progenitor cell line (CG-4) as well as in rat O-2A progenitor cells and oligodendrocytes. O-2A progenitor cells expressed only TR alpha-mRNAs, whereas oligodendrocytes and type 2-astrocytes also expressed TR beta 1-mRNAs. The differential expression of alpha 1 and beta 1 TRs suggests specific functions for both types of TRs during oligodendrocyte differentiation. We present evidence for a possible role of TR alpha 1 in the effect of thyroid hormones on the proliferation of CG-4 cells maintained as progenitor cells.

It is generally accepted that L-3,5,3'-triiodothyronine (L-T3) acts at the genomic level through an interaction with specific nuclear L-T3 receptors (NT3R). Using antibodies raised against different peptides of NT3R, we report here the immunocytochemical localization of the alpha, alpha 2, beta 1 NT3R subtypes in ependymal cell primary cultures. The alpha and beta thyroid hormone receptors are both expressed. While the alpha and alpha 2 subtypes are found in almost all cells, the beta 1 receptors are present in few cells only. The possibility that alpha and beta receptors are colocalized is discussed. We also demonstrate that ependymal cells respond to L-T3 with a marked increase of the expression of the glutamine synthetase messenger RNAs.It is generally accepted that L-3,5,3'-triiodothyronine (L-T3) acts at the genomic level through an interaction with specific nuclear L-T3 receptors (NT3R). Using antibodies raised against different peptides of NT3R, we report here the immunocytochemical localization of the alpha, alpha 2, beta 1 NT3R subtypes in ependymal cell primary cultures. The alpha and beta thyroid hormone receptors are both expressed. While the alpha and alpha 2 subtypes are found in almost all cells, the beta 1 receptors are present in few cells only. The possibility that alpha and beta receptors are colocalized is discussed. We also demonstrate that ependymal cells respond to L-T3 with a marked increase of the expression of the glutamine synthetase messenger RNAs.