细胞间黏附分子-1的研究概况及临床意义

细胞间黏附分子-1( ICAM-1)是一种细胞表面的跨膜糖蛋白,可介导细胞与细胞间或细胞与细胞外基质之间的相互作用.ICAM-1广泛地参与细胞黏附、炎症的发生发展、信号转导和肿瘤转移等多种重要的生理及病理过程.在临床上,ICAM-1可作为多种炎症或肿瘤发展和预后的重要生物标记物之一.以ICAM-1为靶点的药物或能预防和治疗多种急、慢性炎症引起的组织损伤和肿瘤等.     

细胞间黏附分子-1基因多态性与疾病易感性

细胞间黏附分子-1(ICAM-1)属于免疫球蛋白超家族成员之一,是一种细胞表面单链糖蛋白,它表达于多种细胞表面,通过识别其受体LFA-1、MAC-1、P150、P95介导细胞-细胞间的黏附,参与多种炎症反应及免疫过程。不同种族和地区研究证实ICAM-1基因多态性与人类多种疾病相关。     

细胞间黏附分子-1基因多态性与缺血性心脑血管疾病

细胞间黏附分子-1在炎症早期介导白细胞与受损内皮细胞的黏附，由于其基因多态性影响了缺血性心脑血管疾病的发生和预后，成为研究热点。本文就该研究领域的新进展做一综述。     

细胞间黏附分子-1基因多态性与疾病易感性

细胞间黏附分子-1(ICAM-1)属于免疫球蛋白超家族成员之一，是一种细胞表面单链糖蛋白，它表达于多种细胞表面，通过识别其受体LFA-1、MAC-1、P150、P95介导细胞-细胞间的黏附，参与多种炎症反应及免疫过程。不同种族和地区研究证实ICAM-1基因多态性与人类多种疾病相关。     

细胞间黏附分子-1与血管生成的研究进展

实体肿瘤的生长、浸润和转移均依赖于血管生成这一进程,而血管生成是在一系列生长因子调控下实现的。有资料显示,细胞间黏附分子-1与血管生成有关,它通过与内皮细胞表面上的特异性受体结合而发挥其生物学活性,在某些疾病过程中的血管生成及发生发展过程中起着重要作用。现就细胞间黏附分子-1的生物学特性及与血管生成的关系研究进展概述如下。     

细胞间黏附分子-1基因多态性与缺血性心脑血管疾病

细胞间黏附分子-1在炎症早期介导白细胞与受损内皮细胞的黏附,由于其基因多态性影响了缺血性心脑血管疾病的发生和预后,成为研究热点。本文就该研究领域的新进展做一综述。     

细胞间黏附分子-1与肾缺血再灌注损伤

细胞间黏附分子-1(ICAM-1)与肾脏缺血再灌注损伤的病理生理密切相关。肾缺血后损伤显示,损伤不仅是血供中断后组织缺氧的结果,更有再灌注进程中引起炎症反应的激活过程。浸润的白细胞在再灌注中起有害作用,其为活性氧自由基、蛋白水解酶及细胞因子的一个潜在来源。已有证据证实,ICAM-1在白细胞黏连、募集至炎症组织起关键作用。本文着重探讨ICAM-1在肾缺血再灌注损伤中的作用和意义。     

联胺诱导培养的人内皮细胞表达血管细胞黏附分子-1

细胞黏附分子涉及许多生理和病理过程 ,如动脉粥样硬化 (AS) [1] 。有些因素可能诱导细胞黏附分子的表达 ,如氧化低密度脂蛋白 (oxLDL)诱导培养的内皮细胞表达血管细胞黏附分子 1(VCAM 1) [2 ] 。这提示细胞黏附分子可能是导致AS的一种重要因素。我们拟用氧化剂联胺处理培养的人脐静脉内皮细胞 (HUVEC) ,诱导其脂质过氧化损伤 ,观察其VCAM 1mRNA和蛋白表达 ,为抗氧化剂防治AS提供实验依据。一、材料与方法1 HUVEC培养与分组 :用胰酶消化法获取HUVEC ,培养于M199培养基 (Gibco公司产品 ) ,含 5 %新生牛血清、10 %胎牛血清、5 …     

细胞间黏附分子1与糖尿病肾病

细胞间黏附分子 - 1(ICAM 1)又名CD5 4 ,是广泛表达于各种细胞表面的可诱导的单链跨膜糖蛋白 ,属黏附分子中免疫球蛋白超家族成员。ICAM 1在生理情况下呈低水平表达 ,受到高糖、氧化应激、多种细胞因子等各种刺激因素影响后表达则明显上调。ICAM 1在糖尿病的肾脏中表达显著增加 ,可促进细胞的黏附和浸润 ,在糖尿病肾病和肾小球硬化的进展中起重要作用。     

血管内皮生长因子、细胞间黏附分子1在糖尿病大鼠肾小球的表达

目的 探讨血管内皮生长因子(VEGF)和细胞间黏附分子1(1CAM-1)在糖尿病肾病(DN)发生机理中的作用。方法 采用链脲佐菌素(STZ)诱发糖尿病(DM)大鼠模型，观察大鼠肾小球肥大、肾功能和24h尿蛋白改变以及用免疫组织化学和计算机图像分析技术定位、半定量检测VEGF和ICAM—1在DM大鼠肾小球的表达。结果 VEGF和ICAM—1在糖尿病大鼠肾小球中均有不同程度表达，VEGF主要分布于肾小球脏层上皮细胞的脑浆之中，ICAM—1主要分布于肾小球内皮细胞和系膜细胞的脑浆中。VEGF、ICAM-1水平与蛋白尿和肾小球肥大呈正相关关系。结论 DM大鼠肾小球VEGF和ICAM-1的升高可能参与了DN的疾病发展过程，估计是糖尿病肾病发生机理之一。     

sICAM-1和sVCAM-1与乙肝病毒标志物关系的研究

目的探讨可溶性血管内皮细胞问黏附分子1(sVCAM-1)和可溶性细胞问黏附分子1(sICAM-1)的水平与乙肝病毒标志物之间的关系。方法用ELISA法测定乙肝病毒标志物、sVCAM-1、sICAM-1，用PER法定量测定HBV-DNA的含量。结果HBVM阳性者，除HBsAb阳性者外，其血清sVCAM-1、sICAM-1水平较全阴性者均有较明显的升高，但升高的各组间无明显差异；sICAM-1与ALT呈正相关(r=0．652)，与HBA-DNA呈负相关(r=-0．498)；sVCAM-1与ALT、HBV-DNA的相关系数r分别为0．191、-0．027。结论1、乙肝病毒感染者血清sVCAM-1、sICAM-1有明显的升高，各组间无明显差异。2、sICAM-1的水平可以反应肝脏的损害程度和HBV-DNA的复制情况。     

STAT-1对急性胰腺炎大鼠胰腺组织ICAM-1表达的影响

目的:探讨信号转导与转录激活因子-1(STAT-1)在大鼠急性胰腺炎胰腺组织中不同时间点的变化及对细胞黏附分子-1(ICAM-1)表达的影响。方法:36只Wistar大鼠随机分为假手术组(SO组)和急性胰腺炎模型组(AP组)。胆胰管逆行注射5%牛磺胆酸钠制备急性胰腺炎模型。造模后3、6、12h取材,同时观察胰腺组织病理评分,免疫组化SABC法检测不同时间点胰腺组织磷酸化STAT-1和ICAM-1的表达。结果:AP组各时间点胰腺病理评分、磷酸化STAT-1和ICAM-1的表达明显高于SO组(P<0.01);AP组磷酸化STAT-1表达在3h达高峰,后逐渐下降;ICAM-1阳性表达随时间延长逐渐增强,12h达高峰。结论:胰腺炎大鼠胰腺组织STAT-1的活化直接或间接上调ICAM-1的表达可能在其发病过程中起到一定的作用。     

氟伐他汀对缺血再灌注损伤兔心肌细胞间粘附分子的影响

目的:探讨氟伐他汀短期预处理对缺血再灌注损伤兔心肌的保护作用及其机制。方法:日本大耳白兔21只随机分为3组:①假手术对照组(Sham组),②缺血再灌注组(IR组),③氟伐他汀干预组(F组)。实验中持续监测左室收缩压(LVSP)、左室舒张末压(LWEDP)、左室内收缩压最大上升速率和下降速率(±dp/dtmax)的变化,再灌注结束后用伊文氏蓝和TTC染色法确定缺血和梗死心肌范围,用RT-PCR进行心肌局部ICAM-1 mRNA表达测定。结果:缺血再灌注后,F组上述心功能各项指标较IR组明显改善,心肌组织ICAM-1 mRNA水平较IR组显著降低;心肌梗死面积较IR组明显减小。结论:氟伐他汀短期预处理可降低心肌缺血再灌注后心肌ICAM-1 mRNA表达,降低心肌梗死程度,改善心功能,对心肌缺血再灌注损伤有明显的保护作用。     

细胞间粘附分子在脑血管内皮细胞的表达

本文用细胞培养方法，观察脑血管内皮细胞粘附分子（ＩＣＡＭ－１）的表达和内皮细胞与血液单核细胞的粘附作用。结果证实，ＴＮＦ－α，ＩＬ－１和ＩＦＮ可使ＳＨＲ和ＷＫＹ脑血管内皮细胞ＩＣＡＭ－１表达和单核细胞粘附增加，两组动物细胞相比，ＳＨＲ内皮细胞ＩＣＡＭ－１表达及粘附率增加较多，提示ＳＨＲ脑血管内皮细胞可能对细胞因子的敏感性升高。     

Subcellular Localization of Intercellular Adhesion Molecule-1 in Colonic Mucosa in Ulcerative Colitis

Intercellular adhesion molecule-1 (ICAM-1) mediates the firm adhesion of leukocytes to endothelial cells. In ulcerative colitis (UC), ICAM-1 is suggested also to be involved in the further migration of leukocytes toward the epithelial lining, and in colonic tissue it has been reported to be expressed by cell types other than endothelial cells. This study aimed at determining the ultrastructural localization of ICAM-1 on cells belonging to the colonic mucosa from patients with UC. Colonic biopsies from 3 UC patients and 3 control subjects were examined ultrastructurally by immunogold labeling of ICAM-1. ICAM-1 was expressed on the luminal cell membranes of endothelial cells in both controls and inflamed and noninflamed UC colon, although the density was significantly increased in UC ( p <. 0001). Labeling was observed on the basal endothelial cell membranes and on macrophages and plasma cells in inflamed UC colon only. Epithelial cells did not express ICAM-1. ICAM-1 appears to be constitutively upregulated on the luminal endothelial membrane in UC, and the expression on basal endothelial membranes in active UC only suggests that ICAM-1 is more extensively involved in the leukocyte migration than previously acknowledged.     

Soluble Intercellular Adhesion Molecule-1 Serum Profile in Physiologic and Preeclamptic Pregnancy

PROBLEM: The aim of this study was to determine serum levels of soluble intercellular adhesion molecule (sICAM)-1, an adhesion receptor that mediates interactions with the immune system, in physiologic and preeclamptic pregnancies. Moreover, we evaluated whether the release of sICAM-1 during pregnancy correlated to plasma fibronectin concentrations. METHOD OF STUDY: Serum was collected from 18 nonpregnant, control women, from 58 normal pregnant women during the first (n = 13), second (n = 15), and third (n = 30) trimesters, and from 25 preeclamptic patients at 27–39 weeks' gestation. All samples were assayed for sICAM-1 by a specific enzyme-linked immunoassay and for fibronectin by a nephelometric system. Serum sICAM-1 levels in preeclamptic patients were compared to those obtained from gestational-matched normal pregnant women. RESULTS: Levels of sICAM-1 were significantly elevated (P < 0.001) in each of the three trimesters of normal pregnancy (I trimester: 390.4 ± 25.7 ng/ml; II trimester: 386.3 ± 15.4 ng/ml; and III trimester: 367.3 ± 15.8 ng/ml) when compared to those of healthy nonpregnant women (263.3 ± 11.6 ng/ml). No significant difference in sICAM-1 concentrations was observed among the three trimesters. Preeclampsia was associated to a significant decrease (P < 0.01) of sICAM-1 levels (309.8 ± 11.6 ng/ml) relative to those observed in gestational-matched pregnant women (367.3 ± 15.8 ng/ml). Fibronectin and sICAM-1 levels did not correlate. CONCLUSION: The increased levels of sICAM-1 found in physiologic pregnancies and its reduction in preeclampsia may account for some of the immunologic alterations demonstrated to be associated with pregnancy.     

Expression of Intercellular Adhesion Molecule-1 (ICAM-1) on Cultured Human Endometrial Stromal Cells and Its Role in the Interaction With Natural Killers

PROBLEM: Recent evidence emphasizes the role of natural killer cells (NKs) as potential effectors of peritoneal immune surveillance directed against the outgrowth of endometrial cells, refluxed with menstrual debris, in ectopic sites. This NK-mediated cytotoxicity toward autologous endometrial antigens seems to be significantly decreased in endometriosis patients. METHOD: We set up experiments to clarify which molecules are involved in NK-endome-trial cell interaction. In particular, we evaluated the surface expression and functional activity of intercellular adhesion molecule-1 (ICAM-1), a cell surface glycoprotein that has been identified as one of the ligands for lymphocyte function-associated antigen-1 (LFA-1), present on almost all leucocyte cell types. Immunofluorescence flow cytometry was used to assess ICAM-1 expression on resting and IL 1β-activated endometrial stromal cells in culture. Dermal fibroblasts were used as control cells. Cytotoxicity and binding assays by ⁵¹Cr release in presence and absence of a specific monoclonal antibody (mAb) against ICAM-1 were then performed in order to determine the effect of this molecule on NK-mediated cytotoxic and binding activity toward endometrial stromal cells. RESULTS: The results of this study indicated that ICAM-1 expression on endometrial stromal cells seems to be constitutively higher than on dermal fibroblasts and can be up-regulated upon exposure to IL 1β. Furthermore, a mAb against ICAM-1 strongly inhibits the binding but not the cytotoxicity of NKs toward endometrial cells. No difference in the expression of this molecule was observed throughout the cycle. CONCLUSIONS: The presence of ICAM-1 on human endometrium might relate to the action of the immunocompetent cells in human specific reproductive events.     

蛛网膜下腔出血后基底动脉细胞间粘附分子-1的表达

目的：探讨蛛网膜下腔出血（SAH）后迟发性脑血管痉挛的病理过程中细胞间粘附分子－1（ICAM－1）与其发生时相间的关系。方法：采用49只雄性SD大鼠，随机分为实验组和对照组，实验组按存活时间分为6组，采用经额钻孔、注血的方法制作SAH动物模型。切取基底动脉，分别行HE染色和ICAM－1免疫组化染色，进行体视学图像分析。结果：病理切片经图像分析，在SAH后1h和48h管腔面积显缩小（P＜0．001），48h后基底动脉壁发生明显病理形态学变化。SAH后3h血管内皮细胞ICAM－1表达逐渐增强，48h后达到高峰。结论：SAH后可引发急性脑血管痉挛和迟发性脑血管痉挛。ICAM－1参与的炎症反应在SAH后迟发性脑血管痉挛的形成和发展过程中发挥关键性作用。     

原发性肝癌患者血清可溶性细胞间粘附分子-1检测

应用酶联免疫吸附法检测了３８例原发性肝癌（ＰＨＣ）患者血清ｓＩＣＡＭ－１含量,结果表明：⑴ＰＨＣ患者血清ｓＩ ＣＡＭ－１水平明显高于健康对照,肿瘤直径≥５ｃｍ或结节≥３个组血清ｓＩ ＣＡＭ－１水平高于肿瘤直径〈５ｃｍ或结节〈３个组,静脉癌栓形成组（Ｐ均小于０．００１）;⑵ＰＨＣ患者血清ｓＩ ＣＡＭ－１水平与血清Ｂｉｌ－Ｔ、ＡＳＴ含量呈明显正相关（Ｐ〈０．０５）,而与血清ＡＦＰ含量无明显正相关（Ｐ〉