Am J Physiol Cell Physiol AJP: Cell Physiology
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Am J Physiol Cell Physiol 268: C1040-C1044, 1995;
0363-6143/95 $5.00
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AJP - Cell Physiology, Vol 268, Issue 4 C1040-C1044, Copyright © 1995 by American Physiological Society

ARTICLES

Regulation of mouse beta 3-adrenergic receptor gene expression and mRNA splice variants in adipocytes

J. G. Granneman and K. N. Lahners
Department of Psychiatry and Behavioral Neuroscience, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

This study examined the regulation of murine beta 3-receptor mRNA and determined whether the recently described mRNA splice variants are differentially regulated by agents that alter total beta 3-receptor mRNA levels. In vivo treatment of mice with the beta 3-receptor agonist BRL-26830 reduced total beta 3-transcripts by 64% in white adipose tissue but did not alter the mRNA splicing pattern. Further analysis in cultured 3T3-F442A adipocytes showed that isoproterenol, dexamethasone, or phorbol 12-myristate 13-acetate also greatly reduced beta 3-receptor mRNA levels without selectively altering poly-U-containing transcripts. Blockade of transcription with actinomycin D produced a rapid loss of beta 3-receptor mRNA, which was prevented by blockade of mRNA translation with cycloheximide. However, neither actinomycin D nor cycloheximide altered the splicing pattern of beta 3-receptor mRNA. Analysis of transcription rate by nuclear run-off assay indicated that 8-bromoadenosine 3',5'-cyclic monophosphate and phorbol 12-myristate 13-acetate reduce beta 3-receptor gene transcription and that suppression of transcription is sufficient to account for the reduction in beta 3-receptor mRNA levels by these agents.


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Physiol Rev, January 1, 2004; 84(1): 277 - 359.
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