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The Journal of Immunology, 1999, 163: 2151-2159.
Copyright © 1999 by The American Association of Immunologists

Human IL-3 Stimulates Endothelial Cell Motility and Promotes In Vivo New Vessel Formation1

Patrizia Dentelli*, Lorenzo Del Sorbo{dagger}, Arturo Rosso*, Annarita Molinar*, Giovanni Garbarino*, Giovanni Camussi*, Luigi Pegoraro2,* and Maria Felice Brizzi*

Dipartimento di * Medicina Interna, and {dagger} Fisiopatologia Clinica,Università di Torino, Torino, Italy

Angiogenesis is a critical process for growth of new capillary blood vessels from preexisting capillaries and postcapillary venules, both in physiological and pathological conditions. Endothelial cell proliferation is a major component of angiogenesis and it is regulated by several growth factors. It has been previously shown that the human hemopoietic growth factor IL-3 (hIL-3), predominantly produced by activated T lymphocytes, stimulates both endothelial cell proliferation and functional activation. In the present study, we report that hIL-3 is able to induce directional migration and tube formation of HUVEC. The in vivo neoangiogenetic effect of hIL-3 was also demonstrated in a murine model in which Matrigel was used for the delivery of the cytokine, suggesting a role of hIL-3 in sustaining neoangiogenesis. Challenge of HUVEC with hIL-3 lead to the synthesis of platelet-activating factor (PAF), which was found to act as secondary mediator for hIL-3-mediated endothelial cell motility but not for endothelial cell proliferation. Consistent with the role of STAT5 proteins in regulating IL-3-mediated mitogenic signals, we herein report that, in hIL-3-stimulated HUVEC, the recruitment of STAT5A and STAT5B, by the ß common (ßc) subunit of the IL-3R, was not affected by PAF receptor blockade.




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