Altered growth hormone-releasing hormone mRNA expression in transgenic mice with excess or deficient endogenous growth hormone

Molecular and Cellular Neurosciences
D L Hurley, C J Phelps

Abstract

Hypothalamic expression of growth hormone-releasing hormone (GHRH) mRNA was examined in two transgenic mouse models displaying excess or deficient endogenous GH. Transgenic dwarf mice bore a gene construct consisting of the rat growth hormone (GH) promoter fused to a diphtheria toxin A chain structural gene (DT-A); the GH promoter restricted DT-A expression to endogenous GH-producing cells, which were destroyed. GH was undetectable in either the pituitary or the peripheral circulation (Behringer et al., Genes Devel. 2: 453-461, 1988). Transgenic giant mice carried a construction joining the metallothionein promoter to the human GHRH structural gene, which stimulated endogenous pituitary GH production (Hammer et al., Nature 315: 413-417, 1985). In situ hybridization to GHRH mRNA in transgenic dwarf, giant, and nontransgenic controls was performed using single-stranded RNA probes generated from cloned mouse GHRH cDNA. Hybridization to GHRH mRNA was limited to the neurons of the hypothalamic arcuate nucleus (ARC). Autoradiographic densities on X-ray films were quantified by computerized image analysis. There was an increase in GHRH signal intensity in the dwarfs (282 +/- 20 units; mean +/- SEM) relative to that measured in control...Continue Reading

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