HUMAN CEREBROMICROVASCULAR ENDOTHELIUM--DISTINCT PEPTIDERGIC RESPONSES IN VITRO

循环白细胞与血管内皮细胞的黏附是一种 移居到血管外组织的先决条件。数据 展示了细胞间黏附分子-1 (ICAM-1)和血管黏附分子-1(VCAM-1)是构成 人脑内皮细胞系(HBEC)的表达 和脐带静脉(HUVEC)。脂多糖、肿瘤坏死 人脐静脉内皮细胞和人脐静脉内皮细胞的α-因子或干扰素-γ处理 LINES在一段时间内上调了这些黏附分子的表达- 和剂量依赖的方式。同样的促炎因子也 诱导人脐静脉内皮细胞和血管内皮细胞E-选择素的表达 文化。内皮素(ET-1、ET-2和ET-3)也有类似的作用 三种黏附分子在HBEC上的表达然而，一个也没有 对ICAM-1、VCAM-1或E-选择素的影响 HUVEC的表达，尽管伴随着 上述因素对相同文化的影响。这些结果表明 来自不同解剖位置的内皮细胞对 不同于血管活性多肽，内皮素，和牵连 不同来源内皮细胞的作用差异(S) 外周血细胞募集的解剖学定位 发炎。

The adhesion of circulating leukocytes on vascular endothelium is a prerequisite for their emigration to extravascular tissues. The data presented here demonstrate that intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) are constitutively expressed on endothelial cell lines derived from both human brain (HBEC) and umbilical cord veins (HUVEC). Lipopolysaccharide, tumor necrosis factor-alpha or interferon-gamma treatment of both HBEC and HUVEC cell lines up-regulated the expression of these adhesion molecules in a time- and dose-dependent manner. These same pro-inflammatory factors also induced the expression of E-selectin on both HBEC and HUVEC cell cultures. Endothelins (ET-1, ET-2, and ET-3) also had a similar effect on the expression of all three adhesion molecules on HBEC. However, none of the endothelins had any effects on ICAM-1, VCAM-1, or E-selectin expression by HUVEC, despite the concomitant effects of the aforementioned factors on identical cultures. These results indicate that endothelial cells derived from various anatomic locations respond differently to the vasoactive peptide, endothelin, and implicate variations in the role(s) of endothelial cells derived from different anatomic locations in recruitment of blood cells at sites of inflammation.