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J. Biol. Chem., Vol. 279, Issue 22, 23766-23772, May 28, 2004

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Laminin-1 Promotes Angiogenesis in Synergy with Fibroblast Growth Factor by Distinct Regulation of the Gene and Protein Expression Profile in Endothelial Cells^*

Johan Dixelius, Lars Jakobsson, Elke Genersch¶, Svante Bohman, Peter Ekblom, and Lena Claesson-Welsh||

From the Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Dag Hammarskjöldsvaüg 20, S-751 85 Uppsala, Sweden and Section for Cell and Developmental Biology, Biomedicinskt Centrum B12, Lund University, Sölvegatan 19, S-221 84 Lund, Sweden

Laminins are widely distributed extracellular matrix proteins. Certain laminin isoforms are predominant in vascular basement membranes and may be critical in maintaining the stability of the mature vessel. On the other hand, formation of new vessels during angiogenesis requires degradation of the basement membrane, exposing the endothelial cells to other laminin isoforms in the surrounding extracellular matrix. We studied the effects of laminin-1 (LN-1) in different in vitro and in vivo models for angiogenesis. LN-1 induced angiogenesis in the chicken chorioallantoic membrane to the same extent as fibroblast growth factor-2 (FGF-2), and vascular development in embryoid bodies was stimulated in a synergistic manner by FGF-2 and LN-1. LN-1 promoted differentiation of endothelial cells in three-dimensional collagen gels, both in the absence and presence of FGF-2. Formation of tubular structures induced by LN-1 was accompanied by increased expression of Jagged-1, a marker of endothelial differentiation, and increased levels of FGF-2 and FGFR-1 transcripts. LN-1 did not regulate signal transduction pathways known to operate down stream of FGF-2. Thus, phosphorylation of ERK was detected in FGF-2- but not in LN-1-treated cells. Taken together, this suggests that laminins may play a fundamental role in angiogenesis by directly affecting gene and protein expression profiles in endothelial cells.

Received for publication, October 24, 2003 , and in revised form, January 20, 2004.

^* This study was supported by the Swedish Cancer Foundation, the Novo Nordisk Foundation (to L. C.-W. and P. E.), the Swedish Science Council (K2002-99SX-14479-01A and K2002-71X-12552-05A), the Crafoord Foundation (to P. E. and E. G.), and the Pharmacia Corporation (to L. C.-W. and J. D.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ Present address: Institute for Bee Research, Friedrich-Engels-Strasse 32, D-16540 Hohen Neuendorf, Germany.

^|| To whom correspondence should be addressed. Fax: 46-18-55-89-31; E-mail: Lena.Welsh{at}genpat.uu.se.

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