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Variation in Insulin Receptor Messenger Ribonucleic Acid Expression in Human and Rodent Tissues

Barry J. Goldstein^*, Dirk Muller-Wieland and C. Ronald Kahn

Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School Boston, Massachusetts 02215

Address requests for reprints to: Dr. C. Ronald Kahn, Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02215.

Abstract

The expression of insulin receptor mRNA was studied in human and rodent tissues by Northern analysis. Human EBV-transformed lymphocytes contained four receptor mRNA species of sufficient length to encode the entire proreceptor: 9.5, 7.9, 7.1, and 5.7 kb. In human fibroblasts, the same four species were observed; however, the 7.9 and 5.7 kb mRNAs were markedly decreased. In mouse liver, rat hepatoma cells, and normal rat brain, kidney, liver, and muscle only two mRNA species (7.4 and 9.6 kb) were detected. Each of these human and rodent mRNAs hybridized equally well with cDNA sequences encoding the binding and kinase domains of the insulin receptor. Several smaller polyadenylated mRNAs (1.8 to 3.3 kb) were also identified in human cell lines that appeared to separately encode either - or β-subunit sequences of the receptor. In rats, liver had the highest content of insulin receptor mRNA, followed by kidney, brain, and muscle. The relative amount of the two mRNA species also varied among the rat tissues. The ratio of the 9.6–7.4 kb species was 2.7 in brain but only 1.0 to 1.6 in the other tissues (P < 0.025). Dexamethasone treatment increased the content of the two insulin receptor mRNAs in rat liver by 2-fold. The half-life of both mRNA species was 70 min in rat hepatoma cells. These findings indicate that insulin receptor gene expression is complex and regulated with differential expression of insulin receptor mRNA and/or alterations in mRNA processing among various tissues.

FOOTNOTES

This study was supported in part by NIH Grants DK-31036 (to C.R.K.) and DK-33201 (to C.R.K.), the Diabetes Endocrinology Research Center Grant DK-35836, and a Pfizer Biomedical Research Award (to C.R.K.).

^* Pfizer Postdoctoral Fellow in Diabetes.

Recipient of a fellowship of the Deutsche Forschungsgemeinschaft.

Received for publication August 23, 1987. Accepted for publication September 8, 1987.

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