摘要
目的探讨细胞间粘附分子（ＩＣＡＭ－１）是否介导缺氧－再氧化引起的中性粒细胞（ＰＭＮ）和血管内皮细胞（ＶＥＣ）的粘附反应。方法血管内皮细胞（ＶＥＣ）经缺氧再氧化（Ｈ／Ｒ）处理后，加入ＰＭＮ，用计数法检测粘附率，以细胞免疫化学及原位杂交法检测ＩＣＡＭ－１及ＩＣＡＭ－１ｍＲＮＡ表达。结果ＶＥＣ经Ｈ／Ｒ处理后，ＰＭＮ与其粘附率增高１倍（Ｐ＜０．０１），ＩＣＡＭ－１单克隆抗体（ｍＡｂ）与ＣＤ１１ａ／ＣＤ１８ｍＡｂ可明显降低粘附率的增高，Ｈ／Ｒ能增加ＶＥＣ的ＩＣＡＭ－１及ＩＣＡＭ－１ｍＲＮＡ表达。结论ＩＣＡＭ－１介导Ｈ／Ｒ后的ＰＭＮ－ＶＥＣ间粘附反应。
Objective To determine whether intercellular adhesion molecule 1 (ICAM 1) mediats the polymorphonuclear leukocyte (PMN) adherence to endothelial cells elicited by hypoxia/reoxygenation (H/R). Methods Human umbilical vein endothelial cells (HUVEC) monolayers was exposed to hypoxia for 30 min or 120 min then reoxygenated. Count the number of PMN in adhesion assays.Expression of ICAM 1 and ICAM 1 mRNA was detected by immunohistochemical analysis and in situ hybridization. Results PMN adhesion to HUVEC exposed to H/R was significantly increased (1 fold) as compared with that of control(P<0 01). H/R induced hyperadherence was significantly diminished by monoclonal antibodies directed at ICAM 1 or CD11a/CD18.The results showed an increased expression of ICAM 1 and ICAM 1 mRNA on HUVEC exposed to H/R. Hypoxic HUVEC might be responsible for PMN adhesion.Conclusions ICAM 1 mediated the adhesive interaction between PMN and VEC induced by hypoxia/reoxygenation.
出处
《中国医学科学院学报》
CAS
CSCD
北大核心
1999年第2期130-133,共4页
Acta Academiae Medicinae Sinicae
基金
国家自然科学基金
关键词
血管内皮细胞
缺氧
再氧化
细胞间粘附分子
vascular endothelial cell
hypoxia/reoxygenation
intercellular adhesion molecule
