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Transient Stimulation of Myelin Basic Protein Gene Expression in Differentiating Cultured Oligodendrocytes: A Model for 3,5,3'-Triiodothyronine-Induced Brain Development¹

Thyroid Research Unit, Division of Diabetes, Endocrinology and Metabolism, Departments of,Medicine, and Cell Biology and Neuroanatomy, University of Minnesota, Minneapolis, Minnesota 55455

Address all correspondence and requests for reprints to: J. H. Oppenheimer, M.D., University of Minnesota, Box 91-UMHC, Minneapolis, Minnesota 55455. E-mail oppen001{at}maroon.tc.umn.edu

We compared the regulation of myelin basic protein (MBP) gene expression by T₃ in differentiating oligodendrocytes in culture with that previously observed by us in the neonatal rat brain. As in intact brain, expression of the T₃R gene preceded that of the T₃Rß gene. Although the absence of T₃ retarded the rate of accumulation of MBP messenger RNA, the level ultimately attained was similar to that reached in the presence of T₃. This relationship mirrored the pattern observed in the neonatal brain. Transient transfection experiments showed that T₃ regulates MBP expression at the transcriptional level, but only for a limited period during differentiation. These observations imply that the early rise of MBP messenger RNA is T₃ dependent, whereas the terminal levels are maintained independently of T₃. Both the T₃-dependent and, surprisingly, the T₃-independent expression of MBP require the presence of an intact T₃ response element. T₃ receptor may regulate MBP expression in a ligand-independent manner, or a nuclear factor other than T₃ receptor may bind to the T₃ response element of MBP to regulate terminal gene expression. These findings support the use of differentiating oligodendrocytes as a model of T₃-induced brain development.

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