@Article{ecn.2009.0155,
AUTHOR = {Marco Presta, Germán Andrés, Daria Leali, Patrizia Dell’Era, Roberto Ronca},
TITLE = {Inflammatory cells and chemokines sustain FGF2-induced angiogenesis},
JOURNAL = {European Cytokine Network},
VOLUME = {20},
YEAR = {2009},
NUMBER = {2},
PAGES = {39--50},
URL = {http://www.techscience.com/ECN/v20n2/65902},
ISSN = {1952-4005},
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.},
DOI = {10.1684/ecn.2009.0155}
}