Fibroblast Growth Factor-2 (FGF-2) Induces Vascular Endothelial Growth Factor (VEGF) Expression in the Endothelial Cells of Forming Capillaries: An Autocrine Mechanism Contributing to Angiogenesis

doi:10.1083/jcb.141.7.1659

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© The Rockefeller University Press, 0021-9525/1998//1659 $5.00
The Journal of Cell Biology, Volume 141, Number 7, , 1998 1659-1673

Articles

Fibroblast Growth Factor-2 (FGF-2) Induces Vascular Endothelial Growth Factor (VEGF) Expression in the Endothelial Cells of Forming Capillaries: An Autocrine Mechanism Contributing to Angiogenesis

Graziano Seghezzi^*^,, Sundeep Patel^*, Christine J. Ren, Anna Gualandris^||^,¶, Giuseppe Pintucci^||^,¶, Edith S. Robbins^||, Richard L. Shapiro, Aubrey C. Galloway^*, Daniel B. Rifkin^||^,¶, and Paolo Mignatti^*^,^,||

Department of Surgery, ^* Cardiovascular Surgery Research Laboratory and S.A. Localio General Surgery Research Laboratory; and ^|| Department of Cell Biology, and ^¶ the Raymond and Beverly Sackler Foundation Laboratory, and the Kaplan Cancer Center, New York University Medical Center, New York 10016

FGF-2 and VEGF are potent angiogenesis inducers in vivo andin vitro. Here we show that FGF-2 induces VEGF expression invascular endothelial cells through autocrine and paracrinemechanisms. Addition of recombinant FGF-2 to cultured endothelialcells or upregulation of endogenous FGF-2 results in increased VEGF expression. Neutralizing monoclonal antibody to VEGFinhibits FGF-2–induced endothelial cell proliferation.Endogenous 18-kD FGF-2 production upregulates VEGF expressionthrough extracellular interaction with cell membrane receptors;high-M_r FGF-2 (22–24-kD) acts via intracellular mechanism(s).During angiogenesis induced by FGF-2 in the mouse cornea, the endothelial cells of forming capillaries express VEGF mRNAand protein. Systemic administration of neutralizing VEGF antibodydramatically reduces FGF-2-induced angiogenesis. Because occasionalfibroblasts or other cell types present in the corneal stroma show no significant expression of VEGF mRNA, these findingsdemonstrate that endothelial cell-derived VEGF is an importantautocrine mediator of FGF-2-induced angiogenesis. Thus, angiogenesisin vivo can be modulated by a novel mechanism that involvesthe autocrine action of vascular endothelial cell-derived FGF-2 and VEGF.

Abbreviations used in this paper: BAE, bovine aortic endothelial cells; BCE, bovine capillary endothelial cells; DIG, digoxygenin; FGF-2, fibroblast growth factor-2; HAE, human aortic endothelial cells; HMW FGF-2, high molecular weight fibroblast growth factor-2; HUVE, human umbilical vein endothelial cells; LMW FGF-2, low molecular weight fibroblast growth factor-2; rFGF-2, recombinant fibroblast growth factor-2; VEGF, vascular endothelial growth factor; vWF, von Willebrand factor.

Address all correspondence to Paolo Mignatti, Department ofCell Biology, New York University Medical Center, 550 FirstAvenue, New York, NY 10016. Tel.: (212) 263-1478. Fax: (212)263-0147. E-mail: mignap01 @http://mcrcr.med.nyu.edu

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