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(The FASEB Journal. 1998;12:1755-1764.)
© 1998 FASEB

RESEARCH COMMUNICATION

Physiological regulation of hypothalamic TRH transcription in vivo is T3 receptor isoform specific

Hajer Guissoumaa, Mohamed T. Ghorbela, Isabelle Seugneta, Taoufik Ouatasa and Barbara A. Demeneixa,1

a Laboratoire de Physiologie Générale et Comparée, Muséum National d'Histoire Naturelle, URA CNRS 90, 75231 Paris, cedex 5, France

Thyroid hormone (tri-iodo-thyronine, T3) exerts transcriptional effects on target genes in responsive cells. These effects are determined by DNA/protein interactions governed by the type of T3 receptors (TRs) in the cell. As TRs show tissue and developmental variations, regulation is best addressed in an integrated in vivo model. We examined TR subtype effects on thyrotropin-releasing hormone (TRH) transcription and on the pituitary/thyroid axis end point: thyroid hormone secretion. Polyethylenimine served to transfect a TRH-luciferase construct containing 554 bp of the rat TRH promoter into the hypothalami of newborn mice. Transcription from the TRH promoter was regulated in a physiologically faithful manner, being significantly increased in hypothyroidism and decreased in T3-treated animals. Moreover, when various ligand binding forms of mouse or chicken TRß and TR{alpha} were expressed with TRH-luciferase, all forms of TRß gave T3-dependent regulation of TRH transcription, whereas transcription was T3 insensitive with each TR{alpha} tested. Moreover, chicken TR{alpha} increased TRH transcription sixfold, whereas mouse TR{alpha} decreased transcription. These transcriptional effects had correlated physiological consequences: expression of the chicken TR{alpha} in the hypothalamus of newborn mice raised circulating T4 levels by fourfold, whereas mouse TR{alpha} had opposite effects. Thus, TR subtypes have distinct, physiologically relevant effects on TRH transcription.—Guissouma, H., Ghorbel, M. T., Seugnet, I., Ouatas, T., Demeneix, B. A. Physiological regulation of hypothalamic TRH transcription in vivo is T3 receptor isoform specific. FASEB J. 12, 1755–1764 (1998)


Key Words: nonviral gene transfer • polyethylenimine • thyroid hormone • mouse • central nervous system




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