Regulation of mouse [beta]3-adrenergic receptor gene expression and mrna splice variants in adipocytes. Granneman, James G., and Kristine N. Lahners. Cellular and Clinical Neurobiology Program, Department of Psychiatry and Behavioral Neuroscience, Wayne State University School of Medicine, Detroit MI 48201
APStracts 2:0003C, 1995.
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 reatment 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 myristate 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 or cycloheximide altered the splicing pattern of [beta]3 receptor mRNA. Analysis of transcription rate by nuclear run-off assay indicated that 8-bromo-cyclic AMP and phorbol myristate 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. 

Received 8 August 1994; accepted in final form 4 November 1994
APS Manuscript Number C0538-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1994 The American Physiological Society.
Published in APStracts on 27 February 1995.