|
髓磷脂碱性蛋白促进单个核细胞对内皮细胞的粘附效应 |
| |
刘红岩 杨贵贞
摘 要 目的：探讨MBP对外周血单个核细胞(PBMNC)与人脐静脉内皮细胞(HUVEC)粘附性的影响，以揭示中枢神经系统(CNS)炎症时PBMNC进入CNS的可能原因。方法：用细胞粘附试验，研究PBMNC与HUVEC的粘附性，用细胞免疫化学法、FACS分别观察VCAM-1和ICAM-1的表达。结果：MBP活化的PBMNC与MBP刺激的PBMNC培养上清作用的HUVEC的粘附性较对照有显著提高。ICAM-1单抗和可溶性VCAM-1(sVCAM-1)可抑制二者间的粘附。进一步证明该上清可诱导HUVEC表达VCAM-1并可提高ICAM-1的表达量，MBP可刺激PBMNC产生TNF，后者刺激HUVEC产生ICAM-1和VCAM-1，从而促进PBMNC与HUVEC的粘附。结论：MBP可促进PBMNC与HUVEC的粘附，因此在CNS炎症时MBP对PBMNC进入CNS可能起重要作用。
关键词 粘附 细胞间粘附分子-1 血管细胞粘附分子-1 髓磷脂碱性蛋白
中国图书分类号 R392.1
Myelin basic protein promote the effect of peripheral blood mononuclear cells adhesion to human umbilical vein endothelial cells
LIU Hong-Yan，YANG Gui-Zhen.
Department of Immunology，Norman Bethune University of Medical Sciences，Changchun130021
Abstract Objective:To study the influence of MBP to the adhesion of PBMNC to HUVEC，in order to explore possible reason of the PBMNC entering CNS in CNS inflammation.Methods:The adhesion test of cell was used to study the adhesion of PBMNC to HUVEC.Immunocytochemistry and FACS were used to test the expression of ICAM-1 and VCAM-1.Results:Compared with control，much more adhesion cells were showed during PBMNC stimulated by MBP adhesion to HUVEC culturing with the supernatant of MBP stimulating PBMNC.Either anti-ICAM-1 McAb or sVCAM-1 can inhibit the PBMNC-HUVEC adhesion.Furthermore，the supernatant can induce VCAM-1 expression and improve the amount of ICAM-1 on HUVEC.Meanwhile，it was showed that MBP can stimulate PBMNC to secrete TNF.TNF can induce the expression of ICAM-1 and VCAM-1，the latter can promote PBMNC-HUVEC adhesion.Conclusion:MBP can promote the adhesion of PBMNC to HUVEC and may play an important role during PBMNC infiltration to CNS in CNS inflammation.
Key words Adhesion ICAM-1 VCAM-1 MBP
髓磷脂碱性蛋白(myelin basic protein，MBP)是存在于中枢神经系统髓质内的主要蛋白，是引起中枢神经系统炎症的主要自身抗原，在中枢神经系统炎症时，大脑及脊髓的血管周围有大量的单个核细胞浸润，在CNS造成炎性损伤。为了探讨外周血单个核细胞进入CNS的机制，体外研究了MBP对外周血单个核细胞与内皮细胞粘附性的影响，为进一步阐明中枢神经系统炎症[1] [2] 下一页
上一个医学论文： 支气管哮喘发病中 2AR mRNA水平变化的初步探讨
下一个医学论文： 野生型p53基因脂质体转染细胞疫苗的制备
|
|
|
|
|
|
|
您现在的位置： 绿色健康网 >> 医学论文 >> 基础医学论文 >> 正文