کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2131724 | 1086656 | 2011 | 13 صفحه PDF | دانلود رایگان |
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.
Journal: Experimental Cell Research - Volume 317, Issue 1, 1 January 2011, Pages 29–41