Open Access

REVIEW

Inflammatory cells and chemokines sustain FGF2-induced angiogenesis

Marco Presta, Germán Andrés, Daria Leali, Patrizia Dell’Era, Roberto Ronca

Unit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Italy

* Corresponding Author: M. Presta,

European Cytokine Network 2009, 20(2), 39-50. https://doi.org/10.1684/ecn.2009.0155

Accepted 07 April 2009;

Abstract

Angiogenesis and inflammation are closely integrated processes in a number of physiological and pathological conditions, including wound healing, psoriasis, diabetic retinopathy, rheumatoid arthritis, arteriosclero-sis, and cancer. Fibroblast growth factor-2 (FGF2) belongs to the family of the heparin-binding FGF growth factors. FGF2 exerts its pro-angiogenic activity by interacting with various endothelial cell surface receptors, including tyro-sine kinase receptors, heparan-sulfate proteoglycans, and integrins. Elevated levels of FGF2 have been implicated in the pathogenesis of several diseases characterized by a deregulated angiogenic/inflammatory response. FGF2 induces the expression of a wide repertoire of inflammation-related genes in endothelial cells, including pro-inflammatory cytokines/chemokines and their receptors, endothelial cell adhesion molecules, and components of the prostaglandin pathway. Consistent with this pro-inflammatory signature, in vivo evidence points to a non-redundant role for chemokines and infiltrating monocytes/macrophages in FGF2-driven neovascularization. This review will focus on the cross-talk between FGF2 and the inflammatory response in the modulation of blood vessel growth.

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Keywords

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