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J Biol Chem, Vol. 273, Issue 44, 28610-28616, October 30, 1998

The Soluble Type 2 Insulin-like Growth Factor (IGF-II) Receptor Reduces Organ Size by IGF-II-mediated and IGF-II-independent Mechanisms

Silvio Zaina and Sarah Squire

From the Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, United Kingdom

The soluble type 2 insulin-like growth factor (IGF) receptor or IGF-II/mannose 6-phosphate receptor (sIGF2R) is produced in vivo by proteolytic deletion of the transmembrane and intracellular domains of the cellular form of the receptor (IGF2R). There is evidence that sIGF2R is a negative regulator of growth. We have shown that transgenic mice expressing an Igf2r cDNA with a deleted transmembrane domain sequence (sDelta Igf2r) show reduced local organ size. In the present study, we investigate whether sDelta IGF2R can slow the growth induced by an excess of IGF-II and whether the biological activity of sDelta IGF2R is due solely to its interactions with IGF-II. To this end, we crossed sDelta Igf2r transgenics by mice overexpressing IGF-II (Blast line) or by mice carrying a disrupted paternal (active) allele of the Igf2 gene (Igf2m+/p-). Analysis of the phenotypes revealed that the soluble IGF2R affects the size of some organs (colon and cecum) exclusively by reducing the biological activity of IGF-II, whereas in other organs (stomach and skin) the biological activity of the receptor is at least in part independent of IGF-II and must involve an interaction with other factor(s).

Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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