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Molecular and Cellular Biology, October 2004, p. 8662-8670, Vol. 24, No. 19
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.19.8662-8670.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Direct Test of Potential Roles of EIIIA and EIIIB Alternatively Spliced Segments of Fibronectin in Physiological and Tumor Angiogenesis

Sophie Astrof,1 Denise Crowley,1 Elizabeth L. George,2,{dagger} Tomohiko Fukuda,3 Kiyotoshi Sekiguchi,3 Douglas Hanahan,4 and Richard O. Hynes1*

Howard Hughes Medical Institute, Center for Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge,1 Vascular Research Division, Department of Pathology, Brigham and Women's Hospital, Boston Massachusetts,2 Department of Biochemistry and Biophysics, Comprehensive Cancer Center and Diabetes Center, University of California, San Francisco, San Francisco, California,4 Institute for Protein Research, Osaka University, Osaka, Japan3

Received 29 April 2004/ Returned for modification 26 June 2004/ Accepted 13 July 2004

Fibronectin splice variants containing the EIIIA and/or EIIIB exons are prominently expressed in the vasculature of a variety of human tumors but not in normal adult tissues. To understand the functions of these splice variants in physiological and tumor angiogenesis, we used EIIIB-null and EIIIA-null strains of mice to examine neovascularization of mouse retinas, pancreatic tumors in Rip-Tag transgenic mice, and transplanted melanomas. Contrary to expectations, physiological and tumor angiogenesis was not significantly affected by the absence of either EIIIA or EIIIB splice variants. Tumor growth was also not affected. In addition, the expression levels of smooth muscle alpha actin, believed to be modulated by EIIIA-containing fibronectins, were not affected either. Our experiments show that despite their tight regulation during angiogenesis, the presence of EIIIA or EIIIB splice variants individually is not essential for neovascularization.

* Corresponding author. Mailing address: Howard Hughes Medical Institute, Center for Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139. Phone: (617) 253-6422. Fax: (617) 253-8357. E-mail: rohynes{at}mit.edu.

{dagger} Present address: Novartis Institutes for Biomedical Research, Cambridge, MA 02139.

Molecular and Cellular Biology, October 2004, p. 8662-8670, Vol. 24, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.19.8662-8670.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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