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J. Biol. Chem., Vol. 280, Issue 9, 8229-8237, March 4, 2005
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From the Department of Biochemistry and Molecular Genetics, University of Illinois College of Medicine, Chicago, Illinois 60607-7170
The novel angiogenic inducer CCN3 (NOV, nephroblastoma overexpressed) is a matricellular protein of the CCN family, which also includes CCN1 (CYR61), CCN2 (CTGF), CCN4 (WISP-1), CCN5 (WISP-2), and CCN6 (WISP-3). CCN3 is broadly expressed in derivatives of all three germ layers during mammalian development, and its deranged expression is associated with vascular injury and a broad range of tumors. We have shown that CCN3 promotes proangiogenic activities in vascular endothelial cells through integrin receptors and induces neovascularization in vivo (Lin, C. G., Leu, S. J., Chen, N., Tebeau, C. M., Lin, S. X., Yeung, C. Y., and Lau, L. F. (2003) J. Biol. Chem. 278, 24200–24208). In this study, we show that CCN3 is highly expressed in granulation tissue of cutaneous wounds 5–7 days after injury and is capable of inducing responses in primary fibroblasts consistent with wound healing. Purified CCN3 supports primary skin fibroblast adhesion through integrins 
5
1 and 61 and induces fibroblast chemotaxis through integrin v5. We show that CCN3 is a novel ligand of v5 in a solid phase binding assay. Although not mitogenic on its own, CCN3 also enhances basic fibroblast growth factor-induced DNA synthesis. Furthermore, CCN3 up-regulates MMP-1 and PAI-1 expression but interacts with TGF-1 in an antagonistic or synergistic manner to regulate the expression of specific genes. These findings, together with its angiogenic activity, support a role for CCN3 in cutaneous wound healing in skin fibroblasts and establish its matricellular mode of action through integrin receptors.
Received for publication, May 3, 2004 , and in revised form, November 19, 2004.
* This work was supported by National Institutes of Health Grants CA46565 and CA80080 (to L. F. L.). 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.
These authors contributed equally to this work.
Present address: Dept. of Microbiology and Immunology, Vanderbilt University, Nashville, TN, 37332.
¶ Present address: Dept. of Dermatology, Stanford University, 900 Blake Wilbur Dr., Stanford, CA 94305.
|| To whom correspondence should be addressed: Dept. of Biochemistry and Molecular Genetics, University of Illinois, College of Medicine, 900 South Ashland Ave., Chicago, IL 60607-7170. Tel.: 312-996-6978; Fax: 312-996-7034; E-mail: lflau{at}uic.edu.
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