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Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130-3932; and Department of Cardiovascular Research, Genentech, Inc., San Francisco, California 94080
Coordinated
adhesive interactions between lymphocyte receptors and endothelial cell
adhesion molecules (CAMs) are a prerequisite for effector cell entry
into tumor stroma. Whereas the diminished leukocyte-endothelial cell
interactions observed in tumor microvessels have been attributed to a
reduced expression of endothelial CAMs, there is no quantitative data
bearing on this issue. The dual-radiolabeled monoclonal antibody
technique was used to quantify constitutive and tumor necrosis factor
(TNF)-
-induced expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), ICAM-2,
P-selectin, E-selectin, and platelet-endothelial cell
adhesion molecule 1 (PECAM-1) in different vascular beds of normal
(C57Bl/6) and RM-1 tumor-bearing mice. When corrected for endothelial
surface area, the constitutive expression of selectins in tumor vessels
was higher than that observed in other vascular beds. Both constitutive
and induced expression of endothelial CAMs in peripheral vascular beds
did not differ between normal and tumor-bearing mice. Within the tumor,
the magnitude of the upregulation of P-selectin, ICAM-1, and VCAM-1
after TNF- was similar to that within other vascular beds.
E-selectin expression in tumors was refractory to TNF-, whereas
PECAM-1 and ICAM-2 expression were significantly reduced. Our findings
suggest that the presence of a solid tumor does not influence
endothelial CAM expression in other vascular beds and that the higher
density of selectins in nonstimulated tumor vessels may promote the
recruitment of rolling leukocytes in this tissue.
E-selectin; P-selectin; intercellular adhesion molecule 1; vascular cell adhesion molecule 1; platelet-endothelial cell adhesion molecule 1
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