Effect of streptavidin-biotin on endothelial vasoregulation and leukocyte adhesion

被引:13
作者
Chan, BP [1 ]
Reichert, WM [1 ]
Truskey, GA [1 ]
机构
[1] Duke Univ, Durham, NC 27708 USA
关键词
cell adhesion; shear; nitric oxide; leukocyte;
D O I
10.1016/j.biomaterials.2003.10.077
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
The current study examines whether the adhesion promoting arginine-glycine-aspartate-streptavidin mutant (RGD-SA) also affects two important endothelial cell (EC) functions in vitro: vasoregulation and leukocyte adhesion. EC adherent to surfaces via fibronectin (Fn) or Fn plus RGD-SA were subjected to laminar shear flow and media samples were collected over a period of 4 h to measure the concentration of nitric oxide (NO), prostacyclin (PGI(2)), and endothelin-1 (ET-1). Western blot analysis was used to quantify the levels of endothelial-derived nitric oxide synthase (eNOS) and cyclooxygenase 11 (COX 11). In a separate set of experiments, fluorescent polymorphonuclear leukocyte (PMN) adhesion to EC was quantified for EC with and without exposure to flow preconditioning. When cell adhesion was supplemented with the SA-biotin system, flow-induced production of NO and PGI(2) increased significantly relative to cells adherent on Fn alone. Previous exposure of EC to shear flow also significantly decreased PMN attachment to SA-biotin supplemented EC, but only after 2 h of exposure to shear flow. The observed decrease in PMN-EC adhesion was negated by N-G-nitro-L-arginine methyl ester (L-NAME), an antagonist of NO synthesis, but not by indomethacin, an inhibitor to PG, synthesis, indicating the induced effect of PMN-EC interaction is primarily NO-dependent. Results from this study suggest that the use of SA-biotin to supplement EC adhesion encourages vasodilation and PMN adhesion in vitro under physiological shear-stress conditions. We postulate that the presence of SA-biotin more efficiently transmits the shear-stress signal and amplifies the downstream events including the NO and PGI(2) release and leukocyte-EC inhibition. These results may have ramifications for reducing thrombus-induced vascular graft failure. (C) 2003 Elsevier Ltd. All rights reserved.
引用
收藏
页码:3951 / 3961
页数:11
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