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Research Article Free access | 10.1172/JCI113347

Glucocorticoid regulation of insulin receptor gene transcription in IM-9 cultured lymphocytes.

A R McDonald and I D Goldfine

Department of Medicine, Mount Zion Hospital and Medical Center, San Francisco, California 94115.

Find articles by McDonald, A. in: JCI | PubMed | Google Scholar

Department of Medicine, Mount Zion Hospital and Medical Center, San Francisco, California 94115.

Find articles by Goldfine, I. in: JCI | PubMed | Google Scholar

Published February 1, 1988 - More info

Published in Volume 81, Issue 2 on February 1, 1988
J Clin Invest. 1988;81(2):499–504. https://doi.org/10.1172/JCI113347.
© 1988 The American Society for Clinical Investigation
Published February 1, 1988 - Version history
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Abstract

We have reported that glucocorticoids increase steady state insulin receptor mRNA levels in target cells. In the present study using IM-9 cultured human lymphocytes, we investigated the mechanism responsible for this glucocorticoid mediated increase in insulin receptor mRNA levels. Incubation of IM-9 cells with 100 nM dexamethasone for 4 h stimulated a parallel increase in both polysomal and nuclear insulin receptor RNAs indicating that glucocorticoids did not alter the nuclear transport of insulin receptor RNA. Dexamethasone did not alter insulin receptor mRNA half life (t 1/2 = 140 +/- 20 min), indicating that glucocorticoids did not influence mRNA stability. Furthermore, the dexamethasone-induced increase in insulin receptor mRNA levels was not blocked by pretreatment of cells with cycloheximide indicating that the glucocorticoid effect was independent of new protein synthesis. When the labeled transcripts from nuclear run-off incubations were then hybridized to immobilize human insulin receptor cDNA, a three- to fourfold increase in transcriptional activity was observed. This transcriptional effect occurred before the increase in steady state insulin receptor mRNA levels and over the same range of dexamethasone concentrations. These studies indicate therefore a direct effect of glucocorticoids on insulin receptor gene transcription, and demonstrate that the insulin receptor gene is under hormonal control.

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