Tumor angiogenesis and immune response have in common to be cell recognition mechanisms which are based on specific adhesion molecules and dependent on nitric oxide (NO) The aim of the present study is to deepen the mechanisms of angiogenesis and inflammation regulation by NO to find out the molecular regulation processes that govern endothelial cell permeability and leukocyte transmigration Effects of NO either exogenous or produced in hypoxic conditions were studied on microvascular endothelial cells from skin and lymph node because of their strong involvement in melanoma progression We found that NO down-regulation of pseudo-vessel formation was linked to a decrease in endothelial cell ability to adhere to each other which can be explain in part by the inhibition of PECAM-1/CD31 expression On the other hand NO was shown to be able to decrease leukocyte adhesion on an endothelial monolayer performed either in static or in rolling conditions and to modulate differentially CD34 ICAM-1/CD54 ICAM-2/CD102 and VCAM-1/CD106 expression In conclusion during angiogenesis and leukocyte recruitment, NO regulates cell interactions by controlling adhesion molecule expression and subsequently cell adhesion Moreover each endothelial cell type presents its own organospecific response to NO reflecting the functions of the tissue they originate from (C) 2010 Elsevier Inc All rights reserved