Fisp12/Mouse Connective Tissue Growth Factor Mediates Endothelial Cell Adhesion and Migration through Integrin alpha vbeta 3, Promotes Endothelial Cell Survival, and Induces Angiogenesis In Vivo

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Molecular and Cellular Biology, April 1999, p. 2958-2966, Vol. 19, No. 4
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Fisp12/Mouse Connective Tissue Growth Factor Mediates Endothelial Cell Adhesion and Migration through Integrin $alpha$ _v $beta$ ₃, Promotes Endothelial Cell Survival, and Induces Angiogenesis In Vivo

Alexander M. Babic, Chih-Chiun Chen, and Lester F. Lau^*

Department of Molecular Genetics, University of Illinois at Chicago College of Medicine, Chicago, Illinois 60607-7170

Received 18 September 1998/Returned for modification 11 December 1998/Accepted 21 December 1998

Fisp12 was first identified as a secreted protein encoded by a growth factor-inducible immediate-early gene in mouse fibroblasts,whereas its human ortholog, CTGF (connective tissue growth factor),was identified as a mitogenic activity in conditioned media ofhuman umbilical vein endothelial cells. Fisp12/CTGF is a memberof a family of secreted proteins that includes CYR61, Nov, Elm-1,Cop-1/WISP-2, and WISP-3. Fisp12/CTGF has been shown to promotecell adhesion and mitogenesis in both fibroblasts and endothelialcells and to stimulate cell migration in fibroblasts. These findings,together with the localization of Fisp12/CTGF in angiogenic tissues,as well as in atherosclerotic plaques, suggest a possible rolefor Fisp12/CTGF in the regulation of vessel growth during development,wound healing, and vascular disease. In this study, we show thatpurified Fisp12 (mCTGF) protein promotes the adhesion of microvascularendothelial cells through the integrin receptor $alpha$ _v $beta$ ₃. Furthermore,Fisp12 stimulates the migration of microvascular endothelial cellsin culture, also through an integrin- $alpha$ _v $beta$ ₃-dependent mechanism.In addition, the presence of Fisp12 promotes endothelial cellsurvival when cells are plated on laminin and deprived of growthfactors, a condition that otherwise induces apoptosis. In vivo,Fisp12 induces neovascularization in rat corneal micropocket implants.These results demonstrate that Fisp12 is a novel angiogenic inducerand suggest a direct role for Fisp12 in the adhesion, migration,and survival of endothelial cells during blood vessel growth.Taken together with the recent finding that the related proteinCYR61 also induces angiogenesis, we suggest that Fisp12/mCTGFand CYR61 comprise prototypes of a new family of angiogenic regulatorsthat function, at least in part, through integrin- $alpha$ _v $beta$ ₃-dependentpathways.

^* Corresponding author. Mailing address: Department of Molecular Genetics, University of Illinois at Chicago College of Medicine,900 South Ashland Ave., Chicago, IL 60607-7170. Phone: (312) 996-6978.Fax: (312) 996-7034. E-mail: lflau{at}uic.edu.

Molecular and Cellular Biology, April 1999, p. 2958-2966, Vol. 19, No. 4
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

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Fisp12/Mouse Connective Tissue Growth Factor Mediates Endothelial Cell Adhesion and Migration through Integrin v3, Promotes Endothelial Cell Survival, and Induces Angiogenesis In Vivo

Fisp12/Mouse Connective Tissue Growth Factor Mediates Endothelial Cell Adhesion and Migration through Integrin $alpha$ _v $beta$ ₃, Promotes Endothelial Cell Survival, and Induces Angiogenesis In Vivo