Effects of chronic arterial hypertension on constitutive and induced intercellular adhesion molecule-1 expression in vivo
Effects of chronic arterial hypertension on constitutive and induced intercellular adhesion molecule-1 expression in vivo
复制标题
DOI：
10.1161/01.hyp.29.2.683
复制
发表时间：
1997-02-01
期刊：
影响因子：
8.3
通讯作者：
Granger, DN
中科院分区：
文献类型：
--
作者：
Komatsu, S;Panes, J;Granger, DN
最近的报告表明，细菌内毒素（脂多糖）和细胞因子引起的细胞间粘附分子-1（ICAM-1）的表面表达在培养的内皮细胞来自自发性高血压（SHR）与血压正常的Wistar-Kyoto大鼠（WKY）的更深刻的增加。本研究的目的是表征和比较SHR和WKY在基础条件下以及用脂多糖（5 mg/kg IP）或肿瘤坏死因子-α（TNF-α; 1、5和10 μ g/kg IP）激活内皮细胞5小时后的体内ICAM-1表达。ICAM-1的表达定量在不同组织中的双放射性标记的单克隆抗体技术。当组成型（基线）ICAM-1表达校正内皮细胞表面积，显着较高的值比WKY注意到SHR，但仅在内脏器官。脂多糖和TNF-α可引起WKY和SHR所有组织中ICAM-1表达的显著增加。然而，SHR的心脏、胃、骨骼肌和脑中脂多糖诱导的ICAM-1上调幅度显著低于WKY。在给予5 μ g/kg TNF-α后，在SHR的胃中观察到类似的减弱的ICAM-1上调。SHR和WKY之间诱导ICAM-1表达的差异似乎不是由于内皮细胞表面积或血浆糖皮质激素水平的差异。这些结果表明，慢性动脉高血压导致内皮细胞ICAM-1表达改变，这可能有助于与这种疾病相关的异常炎症反应。
Recent reports indicate that bacterial endotoxin (Lipopolysaccharide) and cytokines elicit a more profound increase in the surface expression of intercellular adhesion molecule-1 (ICAM-1) in cultured endothelial cells derived from spontaneously hypertensive (SHR) versus normotensive Wistar-Kyoto rats (WKY). Our objective in this study was to characterize and compare in vivo ICAM-1 expression in SHR and WKY under basal conditions and after 5 hours of endothelial cell activation with either lipopolysaccharide (5 mg/kg IP) or tumor necrosis factor-alpha (TNF-alpha; 1, 5, and 10 mu g/kg IP). ICAM-1 expression was quantified in different tissues by the double-radiolabeled monoclonal antibody technique. When constitutive (baseline) ICAM-1 expression was corrected for endothelial cell surface area, significantly higher values were noted in SHR than WKY but only in splanchnic organs. Lipopolysaccharide and TNF-alpha elicited significant increases in ICAM-1 expression in ail tissues of both WKY and SHR. However, the magnitude of the Lipopolysaccharide-induced ICAM-1 upregulation in heart, stomach, skeletal muscle, and brain was significantly lower in SHR than WKY. A similar blunted ICAM-1 upregulation was noted in the stomach of SHR after administration of 5 mu g/kg TNF-alpha. The differences in induced ICAM-1 expression between SHR and WKY do not appear to be due to differences in endothelial cell surface area or plasma glucocorticoid levels. These results suggest that chronic arterial hypertension results in altered ICAM-1 expression on the endothelium, which may contribute to the abnormal inflammatory responses associated with this disease.