肺腺癌细胞微环境及转移与黏附分子表达的关系

目的研究肺腺癌细胞生长环境及转移性与黏附分子CD44v6和CD29的表达关系。方法将起源相同、转移性不同的两个肺腺癌细胞系AGZY和Anip分别用简便肿瘤多细胞球体(MTS)培养法培养，并设常规单层贴壁细胞培养对照。通过倒置显微镜、扫描及透射电镜观察MTS形成情况，并用免疫组化法分别对MTS及贴壁细胞上CD44v6和CD29表达进行检测。结果MTS培养成功，贴壁细胞与MTS在细胞结构及细胞连接结构上相似，两种MTS在形态及结构上差异无显著性。免疫组化结果显示，CD29在高转移性的Anip细胞及其MTS上呈阳性表达；在低转移性的AGZY细胞及其MTS上阴性表达。CD44v6在Anip和AGZY细胞及MTS上均呈阳性表达，差异无显著性。贴壁细胞与MTS上两种黏附分子表达均无差异。结论成功建立了一种简易制备MTS的方法。细胞生长方式(单层贴壁与MTS)可能不影响CD44v6和CD29的表达。CD29表达可能与肺腺痛转移性相关；CD44v6表达可能与肺腺癌转移无关。     

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.     

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。     

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。     

人细胞间黏附分子-1的真核细胞表达与鉴定

目的 构建人细胞间黏附分子-1(ICAM-1)真核表达载体PcDNA3.1(-)-ICAM-1,并在真核细胞COS-7中表达.方法 设计特异性引物,用PCR方法扩增ICAM-1全编码区基因片段,将其连接人真核表达载体pcDNA3.1(-),并通过酶切进行鉴定.用脂质体转染法将真核表达载体pcDNA3.1(-)-ICAM-1转染COS-7细胞,通过免疫荧光和Western印迹分析人ICAM-1蛋白在COS-7细胞中的表达情况.结果 PCR扩增得到人ICAM-1的cDNA片段大小为1800 bp,重组质粒经酶切鉴定和DNA序列分析确定得到真核表达载体peDNA3.1(-)-ICAM-1.荧光显微镜下可见转染重组质粒的COS-7细胞膜上存在荧光分布,而转染空质粒的细胞未见荧光分布.Western印迹检测发现转染重组质粒的细胞存在外源性的人ICAM-1表达,而转染空质粒的则未见ICAM-1表达.结论 成功构建了人ICAM-1真核表达载体,ICAM-1高效表达在转染的真核细胞COS-7表面,为进一步建立稳定表达ICAM-1的COS-7细胞株以及研究ICAM-1及其受体的生物学功能提供了条件.     

可溶性细胞间黏附分子-1在原发性肝癌患者血清中的表达及其与肝纤维化的关系

目的:探讨可溶性细胞间黏附分子-1(sICAM-1)在原发性肝癌(PHC)患者血清中的水平及其与肝纤维化的关系。方法:采用ELISA方法测定45例PHC患者、30例良性肿瘤患者和35例健康查体者血清sICAM-1和肝纤维化四项(PCⅢ、Ⅳ-C、LN、HA)水平,并分析sICAM-1与肝纤维化之间的关系。结果:PHC组血清sICAM-1和肝纤维化四项(PCⅢ、Ⅳ-C、LN、HA)水平均显著高于良性肿瘤组和正常对照组,相比较有显著性差异(P<0.05);而良性肿瘤组和正常对照组各指标比较差异无统计学意义(P>0.05);血清sICAM-1含量与PCⅢ、Ⅳ-C、LN、HA含量呈显著正相关性(r=0.683、0.575、0.573、0.539,P<0.05)。结论:检测血清sICAM-1的水平对判定PHC患者的病情、为肝癌的早期诊断和治疗有着重要的临床意义。     

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。     

P38 MAPK抑制剂对急性肺损伤大鼠细胞间黏附分子-1表达的影响

目的观察P38 MAPK抑制剂预处理对脂多糖(LPS)致大鼠急性肺损伤(ALI)细胞间黏附分子-1(ICAM-1)的影响,探讨P38 MAPK抑制剂干预ALI的理论基础。方法腹腔内注射 气管内给LPS复制大鼠ALI模型,用免疫组化方法测定肺组织ICAM-1的表达。结果模型组和预处理组的ICAM-1表达显著高于对照组(P<0.01,P<0.05),且模型组高于预处理组(P<0.05)。结论P38MAPK抑制剂预处理可下调大鼠细胞黏附分子ICAM-1的表达,减轻肺组织的病理损害,能起到防治ALI的作用。     

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。     

ICAM-1与支气管哮喘的研究进展

细胞间粘附分子-1(intercellularadhesionmolecule-1,ICAM-1)是免疫球蛋白(immunoglobulin,Ig)超家族成员之一,对白细胞牢固黏附和白细胞从血管中迁移到炎症组织部位起着关键作用.白细胞表面粘附分子与血管内皮细胞表面的粘附分子(如:ICAM-1)相互作用后可介导白细胞从血液循环中迁移到肺组织的炎症部位,这在支气管哮喘发病机制中起着重作用.本综述将简阐述ICAM-1及其表达调控在支气管哮喘中的研究进展.     

Circulating soluble intercellular adhesion molecule-1 (sICAM-1) in patients with sarcoidosis

sICAM-1 has been elevated in sera of specific inflammatory diseases, and circulating sICAM-1 concentrations reflect disease activity in these diseases. We measured circulating sICAM-1 concentrations and serum angiotensin-converting enzyme (SACE) activity in patients with sarcoidosis. Patients with sarcoidosis had significantly increased circulating sICAM-1 concentrations (62.8±33.5U/ml) and SACE activity (23.7±7.4U/l) compared with controls (circulating sICAM-1 50.9±12.1U/ml, and SACE 13.5±3.8U/l). Successive measurements showed that circulating sICAM-1 values changed in parallel with disease activity in sarcoidosis. In the progressive disease group (progressed or without change for 2 years or more), circulating sICAM-1 values (102.2±35.3U/ml) at the time of diagnosis were significantly increased compared with those in the regressive disease group (disappeared or regressed within 2 years) (46.4±12.6U/ml). However, there was no significant difference in SACE activity of the regressive and progressive disease groups. Fifteen patients with a high value of circulating sICAM-1 (> 75U/ml, mean of controls+2s.d.) all had progressive disease, while only 15 of 44 patients with a high value of SACE had progressive disease. Circulating sICAM-1 will be a useful blood marker to predict outcome and to monitor disease activity in sarcoidosis.     

细胞间黏附分子-1基因K469E多态性与类风湿性关节炎的关系

目的 探讨细胞间黏附分子-1(intercelluhr adhesion molecul-1,ICAM-1)基因K469E多态性与类风湿性关节炎(rheumatoid arthritis,RA)的关系.方法 对275例类风湿性关节炎患者和254名体检健康者作为对照组进行研究.采用聚合酶链反应-限制性片段长度多态性方法分析ICAM-1基因K469E的多态性.结果 RA组K469E位点KK、KE和EE基因型频率为0.535、0.411和0.054;健康对照组K469E位点KK、KE和EE基因型频率为0.512、0.437和0.051.RA组K469E基因型频率与健康对照组相比差异无统计学意义(x2=0.371,P=0.831).RA组K等位基因频率(0.74)与健康对照组(0.73)相比差异无统计学意义(x2=0.127,P=0.721,OR=1.051,95%CI为0.800～1.381),在RA组中KK+KE基因型频率与对照组相比,差异无统计学意义(P=0.863,OR=0.935,95%CI为0.436～2.005).结论 ICAM-1基因K469E多态性分布与RA的易感性无明显相关性.

Abstract：

Objective To investigate the association of the intercellular adhesion molecule-1 gene (ICAM-1)K469E polymorphism and rheumatoid arthritis (RA). Methods Two hundred and seventy five patients with RA and 254 healthy individuals were collected and enrolled in the study. The K469E polymorphism of ICAM-1 gene was analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results The genotype frequencies of KK, KE and EE of K469E polymorphism were 0. 535,0.411 and 0. 054 respectively in the RA patients, and 0. 512,0. 437 and 0. 051 respectively in the healthy individuals, and there was no significant difference between the two groups (x2 =0. 371,P=0. 831). The frequencies of the K469 allele were 0. 74 and 0. 73 in the RA patients and the controls respectively (x2 = 0. 127, P = 0. 721, OR = 1.051,95 % CI: 0. 800-1. 381 ). No significant difference was observed in KK+KE genotype frequencies between the two groups (P=0. 863), with an odds ratio of 0. 935 (95% CI: 0. 436-2.005). Conclusion The K469E polymorphism of the ICAM-1 gene was not associated with the susceptibility of rheumatoid arthritis.     

The role of amniotic fluid interleukin-6, and cell adhesion molecules, intercellular adhesion molecule-1 and leukocyte adhesion molecule-1, in intra-amniotic infection

PROBLEM: To determine amniotic fluid concentrations and correlations of interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), and leukocyte adhesion molecule-1 (LAM-1) in patients with and without intra-amniotic infection. METHOD OF STUDY: Fourteen specimens with intra-amniotic infection and 45 without intra-amniotic infection were studied. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture. Amniotic fluid IL-6, ICAM-1, and LAM-1 levels were determined by an enzyme-linked immunoassay, and normalized by amniotic fluid creatinine levels. RESULTS: Amniotic fluid concentrations of IL-6 and LAM-1 were significantly higher in patients with than without intra-amniotic infection. However, amniotic fluid ICAM-1 concentrations were not significantly different between two groups. Amniotic fluid IL-6, LAM-1, and ICAM-1 were positively correlated. CONCLUSIONS: Our data indicate that amniotic fluid IL-6 is significantly associated with an increased adhesion molecule expression in intra-amniotic infection. However, LAM-1 plays a more important role than ICAM-1 in intra-amniotic infection.     

大肠癌患者血清可溶性P-选择素和细胞间黏附分子-1的表达及意义

目的 探讨大肠癌患者手术前后血清可溶性P-选择素（sP-selectin）、细胞间黏附分子-1（sICAM-1）的表达及临床意义。方法 采用ELISA检测30例大肠癌患者术前、术后15日、术后30日及20例对照组血清sP—selectin、sICAM-1的表达水平。结果 ①大肠癌患者血清sP—selectin、sICAM-1的表达水平均显著高于对照组，P〈0.05；术后15日下降，仍高于对照组水平，P〈005；术后30日降至对照组水平，P〉0．05；②大肠癌患者血清sP-selectin、sICAM-1的表达水平与淋巴结转移和临床分期相关，P〈0．05，与年龄、性别、肿瘤大小厦组织学分级无明显相关。P〉O．05。结论 sPselectin、slCAM-1参与了大肠癌侵袭转移过程，是反映大肠癌的发生、发展及预后的一个重要指标。     

Immunohistochemical analysis of intercellular adhesion molecule-1 expression in human gastric adenoma and adenocarcinoma

In this study, we examined the distribution of intercellular adhesion molecule-1 (ICAM-1) in gastric adenomas and carcinomas immunohistochemically at the light and electron microscopic levels. ICAM-1 was expressed on tumour cells in 12 of 28 gastric carcinomas and in 3 of 11 adenomas but not on most normal gastric epithelial cells. ICAM-1 was localized on luminal sites of neoplastic glands in adenomas and in intestinal-type carcinomas, and rarely on the surface of tumour cells of diffuse carcinomas. Expression of ICAM-1 on the tumour cells was more frequent in intestinal-type than diffuse carcinomas (P<0.005). At the ultrastructural level, ICAM-1 was present prominently on the apical membrane and weakly on the lateral surface of the tumour cells of the intestinal-type carcinoma and also localized on the perinuclear membrane and the membrane of the endoplasmic reticulum of cancer cells. There was no significant association between. ICAM-1 expression and HLA antigen expression or the number of infiltrating lymphocyte subsets. These results may implicate the synthesis of ICAM-1 by gastric cancer cells, but the expression is infrequent and may not be sufficient for host immune surveillance of the tumour cell.     

Role of intercellular adhesion molecule-1 in a murine model of toluene diisocyanate-induced asthma

BACKGROUND: Adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) are thought to contribute to the airway inflammation and airway hyper-responsiveness (AHR) of allergic asthma. Some differences from allergic asthma have been noted, including airway neutrophilia, and the involvement of ICAM-1 in toluene diisocyanate (TDI) asthma is currently unclear. OBJECTIVE: We utilized mice lacking ICAM-1 expression (ICAM-1(-/-)) to investigate the role of ICAM-1 in airway inflammation and AHR in TDI-induced asthma. METHODS: Male C57BL/6J mice (ICAM-1(+/+)) and ICAM-1(-/-) mice were intranasally sensitized to TDI solution or solvent alone. Airway inflammation, AHR and cytokine secretion were assessed 24 h after challenge by TDI or solvent. The production of antigen-specific IgG and IgE by TDI sensitized and non-sensitized mice was determined. RESULTS: TDI challenge to ICAM-1(+/+) mice induced an increase in airway inflammatory cell numbers, AHR and cytokine secretion of TNF-alpha, macrophage inflammatory protein-2 (MIP-2), IL-4, IL-5 and IFN-gamma into the bronchoalveolar lavage fluid. All these pathophysiological changes were reduced in ICAM-1(-/-) mice. Serum levels of TDI-specific IgG and IgE of ICAM-1(-/-) and ICAM-1(+/+) mice were comparable. CONCLUSION: These results suggest that ICAM-1 plays an essential role in airway inflammation and AHR in TDI-induced asthma.     

维持性血液透析尿毒症患者sICAM-1和E-选择素水平的变化

目的 :测定维持性血液透析 (MHD)的尿毒症患者血浆中细胞间黏附分子 1(ICAM 1)和E 选择素的水平 ,探讨MHD患者动脉粥样硬化的病理机制。方法 :应用双抗夹心ELISA法 ,测定 10 5例MHD患者和 2 5例健康人 (对照组 )血浆中ICAM 1和E 选择素的水平 ,同时用B超测定患者颈动脉粥样硬化的情况 ,记录两组的血压并测定其血脂、血糖、血尿素和肌酐的水平。结果 :①MHD组血浆ICAM 1和E 选择素的水平均明显高于对照组 (P <0 .0 1)。MHD组中 ,有颈动脉硬化者血浆I CAM 1和E 选择素的水平明显高于无颈动脉硬化组 (分别为P <0 .0 1和P <0 .0 5)。②MHD组血浆ICAM 1与E 选择素以及与甘油三酯 (TG )均呈显著的正相关 (r值分别为0 .62及 0 .60 )。血浆ICAM 1的水平与舒张压也呈正相关(r=0 .41)。结论 :MHD患者存在明显的血管内皮功能损伤。血浆ICAM 1和E 选择素可作为MHD患者血管内皮损伤的标志物 ,其与MHD患者的动脉粥样硬化密切相关     

Increased plasma concentrations of intercellular adhesion molecule-1 after strenuous exercise associated with muscle damage

Intercellular adhesion molecule-1 (ICAM-1) plays an important role in leukocyte migration from the circulation and intervention at sites of inflammation. We investigated the effects of various types of exercise on circulating levels of soluble ICAM-1 (sICAM-1) in normal healthy male adults. Plasma concentrations of sICAM-1 were measured before and after bicycle ergometer exercise at intensity of 80% maximal oxygen consumption ( ) (16 min), 42 km endurance running and 30-min downhill running at intensity of ventilation threshold (VT). The plasma sICAM-1 level increased 1 day after the endurance running (12%) and downhill running (14%), but not after ergometer exercise. Plasma C-reactive protein (CRP) and creatine kinase (CK) concentrations also increased 1 day after running. Our data suggest that exercise associated with muscle damage and/or inflammation results in increased levels of plasma sICAM-1. The physiological significance of post-exercise high plasma sICAM-1 levels is not clear at this stage, but changes in plasma sICAM-1 may reflect the status of the immune system. Electronic Publication     

Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression and function on cultured human glomerular epithelial cells.

Glomerular epithelial cells are involved in extracapillary inflammation (crescents) but the mechanisms of this extracapillary accumulation of macrophages, epithelial cells and occasional lymphocytes are unknown. Human glomerular parietal epithelial cells express ICAM-1 and VCAM-1 on immunohistological stains of renal biopsies. We studied the expression of these cell adhesion molecules on cultured human glomerular epithelial cells (HGEC), their regulation by pro-inflammatory cytokines, and their role in mediating the adhesion of concanavalin A (Con A)-activated peripheral blood mononuclear cells. Human glomerular epithelial cells in culture constitutively express ICAM-1 and VCAM-1. The expression of ICAM-1 was not significantly altered by tumour necrosis factor-alpha (TNF-alpha) (P = 0.32), IL-1 beta (P = 0.24), interferon-gamma (IFN-gamma) (P = 0.66) or IL-4 (P = 0.85). VCAM-1 expression was increased by all four cytokines, but only significantly so by IL-4 (P = 0.0001). Con A-stimulated, monocyte-depleted peripheral blood lymphocytes bound to human glomerular epithelial cells, median 28.9% (range 14.5-37.9%). This adherence was significantly inhibited by anti-ICAM-1 (P = 0.03) and anti-LFA-1 (P = 0.02), but not by anti-VCAM-1 (P = 0.13) or by antibody to von Willebrand factor (P = NS). The interaction between ICAM-1 on HGEC and LFA-1 on mononuclear cells may be important in the pathogenesis of extracapillary inflammation in glomerulonephritis.