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Originally published In Press as doi:10.1074/jbc.M108061200 on November 28, 2001

J. Biol. Chem., Vol. 277, Issue 6, 4505-4511, February 8, 2002
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Insulin-like Growth Factor II Plays a Central Role in Atherosclerosis in a Mouse Model*

Silvio ZainaDagger §, Linda PetterssonDagger , Bo Ahrén, Lena BrånénDagger , A. Bassim Hassan||, Marie LindholmDagger , Ragnar Mattsson**, Johan ThybergDagger Dagger , and Jan NilssonDagger

From the Dagger  Experimental Cardiovascular Research, Wallenberg Laboratory, Department of Medicine, University of Lund, Malmö General Hospital, 205 02 Malmö, Sweden, the  Department of Medicine, BMC, University of Lund, 221 84 Lund, Sweden, the || Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, United Kingdom, the ** Lund Transgenic Core Facility, C13, BMC, University of Lund, 223 62 Lund, Sweden, and the Dagger Dagger  Department of Cell and Molecular Biology, Karolinska Institutet, 171 77 Stockholm, Sweden

Insulin-like growth factor II is a fetal promoter of cell proliferation that is involved in some forms of cancer and overgrowth syndromes in humans. Here, we provide two sources of genetic evidence for a novel, pivotal role of locally produced insulin-like growth factor II in the development of atherosclerosis. First, we show that homozygosity for a disrupted insulin-like growth factor II allele in mice lacking apolipoprotein E, a widely used animal model of atherosclerosis, results in aortic lesions that are ~80% smaller and contain ~50% less proliferating cells compared with mice lacking only apolipoprotein E. Second, targeted expression of an insulin-like growth factor II transgene in smooth muscle cells, but not the mere elevation of circulating levels of the peptide, causes per se aortic focal intimal thickenings. The insulin-like growth factor II transgenics presented here are the first viable mutant mice spontaneously developing intimal masses. These observations provide the first direct evidence for an atherogenic activity of insulin-like growth factor II in vivo.

* This work was supported by the Swedish Heart Lung Foundation, Kungliga Fysiografiska Sällskapet i Lund, Lundströms Stiftelse, Novo Nordic Foundation, Albert Påhlsson Foundation, Swedish Diabetes Association, the King Gustaf V 80th Birthday Fund, and UMAS Forskningsfonder and by Swedish Medical Research Council Grants 6834 (to B. A.), 8311 (to J. N.), and 6537 (to J. T.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed: Experimental Cardiovascular Research, Entrance 46, 1st Fl., Wallenberg Laboratory, Dept. of Medicine, University of Lund, Malmö General Hospital, 205 02 Malmö, Sweden. Tel.: 46-40-337656; Fax: 46-40-332550; E-mail: silvio.zaina@medforsk.mas.lu.se.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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