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J Biol Chem, Vol. 273, Issue 17, 10586-10593, April 24, 1998
From the The objective of this study was to determine the
mechanisms by which cortisol down-regulates hepatic insulin-like growth
factor-II (IGF-II) gene expression in late gestation. Leader exons 6 and 7 of the ovine IGF-II gene, with their 5'-flanking regions, were first isolated. Characterization of transcription start sites revealed
a unique site for exon 6 and three dispersed sites for exon 7. Nuclear
run-on assays showed a 5-fold higher transcription rate of the IGF-II
gene in liver of adrenalectomized fetuses compared with control
animals, suggesting that regulation of IGF-II gene expression by
cortisol is at the transcriptional level. RNase protection assays
demonstrated hepatic leader exon 7 expression in adrenalectomized
fetuses to be more than 2-fold higher than in controls, whereas it was
reduced by 50% in cortisol-infused fetuses compared with controls.
There was no effect on the expression of other leader exons. Functions
of the upstream regulatory region of leader exon 7 (i.e.
promoter P4) were investigated by luciferase transient expression. A
region of
Transcriptional Regulation of Insulin-like Growth Factor-II Gene
Expression by Cortisol in Fetal Sheep during Late Gestation
§,,, and
Department of Cellular Physiology,
172 bases downstream relative to the first transcription
site of leader exon 7 was shown to retain basal promoter activity and
respond to cortisol. These results suggest that cortisol may induce the
prenatal decline in ovine hepatic IGF-II expression by suppressing
promoter P4 of the IGF-II gene.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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