Dramatic pituitary hyperplasia in transgenic mice expressing a human growth hormone-releasing factor gene

Kelly E. Mayo*, Robert E. Hammer, Larry W. Swansont, Ralph L. Brinster, Michael G. Rosenfeld, Ronald M. Evans

*Corresponding author for this work

Research output: Contribution to journalArticle

159 Scopus citations

Abstract

A transgenic animal model system was used to analyze the mitogenic effects of GRF on its target cell, the pituitary somatotroph. We have previously established a strain of mice that express a mouse metallothionein-l/human GRF (hGRF) fusion gene, and that grow to be abnormally large due to GH hypersecretion. We show here that chronic GRF production in these mice leads to the development of enormous pituitary glands. The increase in pituitary size appears to be largely the result of a selective proliferation (hyperplasia) of somatotrophs, the GH-producing cells. This observation provides direct evidence that a neuropeptide may act as a specific trophic factor for its target cell. In addition to this effect on pituitary development, we find that the pituitary is a major site of expression of mouse metallothionein-l/hGRF mRNA, and of hGRF peptide. This tissue specificity was unexpected in that neither component of the fusion gene is highly expressed in the normal pituitary. It suggests that pituitary somatotrophs might produce and respond to GRF in an essentially autocrine fashion in these.

Original languageEnglish (US)
Pages (from-to)606-612
Number of pages7
JournalMolecular Endocrinology
Volume2
Issue number7
DOIs
StatePublished - Jul 1988

ASJC Scopus subject areas

  • Molecular Biology
  • Endocrinology

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