Nitric oxide regulates interactions of PMN with human brain microvessel endothelial cells

被引:13
|
作者
Wong, D
Prameya, R
Dorovini-Zis, K
Vincent, SR [1 ]
机构
[1] Univ British Columbia, Dept Psychiat, Vancouver, BC, Canada
[2] Univ British Columbia, Vancouver Gen Hosp, Sect Neuropathol, Brain Res Ctr, Vancouver, BC V5Z 1M9, Canada
[3] Univ British Columbia, Vancouver Gen Hosp, Sect Neuropathol, Dept Pathol & Lab Med, Vancouver, BC V5Z 1M9, Canada
基金
加拿大健康研究院;
关键词
polymorphonuclear leukocytes; cGMP-dependent protein kinase; adhesion molecules; tumor necrosis factor-alpha; E-selectin; ICAM-1;
D O I
10.1016/j.bbrc.2004.08.062
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The hypothesis that the NO/cGMP pathway modulates PMN adhesion to human brain microvessel endothelial cells (HBMEC) was examined. Human PMN were incubated with resting or TNF-alpha-treated endothelial monolayers, and adhesion was quantified by light microscopy. TNF-alpha upregulated PMN adhesion in a time-dependent manner. Treatment of HBMEC with the NO donors SNP and DETA NONOate for 4 or 24 h decreased PMN adhesion. This was completely reversed by the guanylyl cyclase inhibitor ODQ, while addition of a cGMP agonist (8-Br-cGMP) decreased PMN adhesion. NO donors did not affect the levels of E-selectin or ICAM-1 in HBMEC. However, pre-treatment of PMN with NO donors or 8-Br-cGMP decreased their adhesion to recombinant E-selectin and ICAM-1, suggesting an effect of NO on PMN. These findings indicate that NO modulates PMN-HBMEC interactions through cGMP and decreases the binding of PMN to the adhesion molecules E-selectin and ICAM-1. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:142 / 148
页数:7
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