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 Blood, 15 May 2007, Vol. 109, No. 10, pp. 4264-4271.
Prepublished online as a Blood First Edition Paper on February 8, 2007; DOI 10.1182/blood-2006-06-029603.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

C-KIT, by interacting with the membrane-bound ligand, recruits endothelial progenitor cells to inflamed endothelium

Patrizia Dentelli1, Arturo Rosso1, Antonina Balsamo1, Sofia Colmenares Benedetto1, Annarita Zeoli1, Marco Pegoraro2, Giovanni Camussi1, Luigi Pegoraro1, and Maria Felice Brizzi1

1 Department of Internal Medicine, University of Turin, Italy; 2 Division of Vascular Surgery, Ospedale Molinette, Turin, Italy

We investigated the role of c-Kit and the membrane-bound ligand (mbKitL) in endothelial progenitor cell (EPC) recruitment by microvascular endothelial cells (ECs). We demonstrated that inflammatory activation induced the expression of the mbKitL on ECs both in vitro and in vivo, and that recruitment of EPCs depended on c-Kit/mbKitL interaction. Depletion of endogenous c-Kit or inhibition of c-Kit enzymatic activity by imatinib mesylate prevented adhesion of EPCs to activated ECs both in vitro and in vivo, indicating that a functional c-Kit on EPCs is essential. We also demonstrate that Akt was the downstream molecule regulating cell adhesion. A potential role of the c-Kit/mbKitL interaction in pathological settings is sustained by the expression of the mbKitL on ECs lining intraplaque neovessels. Thus, our results provide new insights into the mechanisms underlying EPC recruitment and the bases for novel strategies to hinder pathological angiogenesis.


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Inflamed endothelium: an EPC adhesion kit
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Blood 2007 109: 4118. [Full Text] [PDF]



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