Nitric oxide reduces endothelial expression of intercellular adhesion molecule (ICAM)-1.
Nitric oxide reduces endothelial expression of intercellular adhesion molecule (ICAM)-1.
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一氧化氮减少内皮细胞间粘附分子 (ICAM)-1 的表达。
DOI：
10.1006/jsre.1996.0270
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Barnett,C
中科院分区：
文献类型：
--
作者：
Biffl,WL;Moore,EE;Moore,FA;Barnett,C
一氧化氮(NO·)已被证实能有效改善急性呼吸窘迫综合征(ARDS)患者的氧合，降低肺动脉高压，但其确切机制尚不清楚。NO·已被证明可减少白细胞与内皮细胞的黏附，减轻中性粒细胞(PMN)的隔离，并保护内皮免受炎性损害。细胞间黏附分子(ICAM)-1是PMN-内皮黏附的关键调节因子，也是PMN细胞毒作用的重要介质。因此，我们假设NO·抑制内皮细胞ICAM-1的表达。培养人脐静脉内皮细胞(HUVEC)。将NO·供体3-吗啉基核苷二亚胺(SIN-1)(0.1~10μM)与人脐静脉内皮细胞孵育4h。在单独的实验中，HUVEC单独与细菌脂多糖(LPS)(100 ng/ml)孵育或在SIN-1预处理后孵育。流式细胞仪检测HUVEC ICAM-1的表达。SIN-1(1和10μM)可使静息状态下脐静脉内皮细胞ICAM-1的表达分别降低58%和47%。脂多糖可上调ICAM-1的表达，但不受SIN-1预处理的影响。我们的结论是，NO·降低了ICAM-1的构成内皮表达，但不能阻止内毒素刺激的ICAM-1的表达上调。下调ICAM-1可能是NO·保护静息内皮细胞(远处器官床)免受循环启动或激活的PMN的一种机制，但在原发炎症部位可能不起作用。
Nitric oxide (NO·) has proven effective in improving oxygenation and reducing pulmonary hypertension in the acute respiratory distress syndrome (ARDS), but the precise mechanism remains unclear. NO·has been shown to reduce leukocyte-endothelial adhesion, attenuate neutrophil (PMN) sequestration, and protect endothelium from an inflammatory insult. Intercellular adhesion molecule (ICAM)-1 is a pivotal regulator of PMN-endothelial adhesion and, thus, a critical mediator of PMN cytotoxicity. Consequently, we hypothesized that NO·suppresses ICAM-1 expression on endothelium. Human umbilical vein endothelial cells (HUVEC) were cultured. The NO·donor 3-morpholinosidnonimine (SIN-1) (0.1–10 μM) was incubated with HUVEC for 4 hr. In separate experiments, HUVEC were incubated with bacterial lipopolysaccharide (LPS) (100 ng/ml) alone or following SIN-1 pretreatment. ICAM-1 expression on HUVEC was measured by flow cytometric analysis. SIN-1 (1 and 10 μM) reduced the expression of ICAM-1 on resting HUVEC by 58 and 47%, respectively. LPS upregulated ICAM-1 expression; however, this was not affected by SIN-1 pretreatment. We conclude that NO·reduces constitutive endothelial expression of ICAM-1, but does not prevent LPS-stimulated upregulation of ICAM-1 expression. Downregulation of ICAM-1 may be a mechanism whereby NO·protects resting endothelium (distant organ bed) from circulating primed or activated PMNs, but may not be as effective at a primary inflammatory site.
影响因子：
20.3
作者：
T. Carlos;J. Harlan
通讯作者：
T. Carlos;J. Harlan
影响因子：
158.5
作者：
ROSSAINT, R;FALKE, KJ;ZAPOL, WM
通讯作者：
ZAPOL, WM