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J. Biol. Chem., Vol. 283, Issue 19, 13148-13155, May 9, 2008

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Fibronectin Type I Repeat Is a Nonactivating Ligand for EphA1 and Inhibits ATF3-dependent Angiogenesis^*

From the Department of Pharmacology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan

ATF3 stimulated promoter activity of EphA1 by 3.4-fold in ATF3-dependent angiogenesis in vitro. Although tyrosine kinase activation of EphA1 was dispensable, binding of EphA1 to fibronectin through its type I repeat played an essential role in the angiogenesis. Recombinant proteins containing fibronectin 10th to 12th type I repeat (I 10–12) but not I 12 could inhibit the angiogenesis in vitro by competitively targeting EphA1 with the full-length fibronectin. However, I 12 acquired a higher affinity toward EphA2 with K_d 18 nM and inhibited vascular endothelial growth factor-dependent angiogenic invasion in a Matrigel plug assay.

Received for publication, March 13, 2007 , and in revised form, January 10, 2008.

^* This work was supported in part by Grant-in-aid for Scientific Research 12147210 (to Y. M.) and by the Center of Excellence Program for the 21st Century in Japan. 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.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. 1–3.

¹ To whom correspondence should be addressed. Tel.: 81-3-5269-7417; Fax: 81-3-5269-7417; E-mail: ymaru{at}research.twmu.ac.jp.