肠癌淋巴管内皮细胞ICAM-1、CEA的表达

肠癌转移的主要途径是淋巴结转移。直接影响患者的预后。而淋巴系统转移首先是癌细胞沿着淋巴管转移 ,淋巴管转移涉及淋巴管内皮细胞与癌细胞的相互作用。这种相互作用的分子基础与细胞粘附分子有关。为此 ,本文运用石蜡切片免疫组化方法 ,研究 ICAM、CEA在淋巴管内皮细胞的表达 ,结果发现转移淋巴管内皮细胞表达 ICAM和 CEA,而正常淋巴管内皮细胞不表达 ICAM和 CEA,提示肠癌淋巴转移与淋巴管内皮细胞分泌 ICAM和 CEA有关     

HIV-1Nef调节内皮细胞黏附分子ICAM-1的表达

目的研究HIV-1的调节基因Nef对ECV304细胞ICAM-1表达的影响,从而为分析HIV-1感染引起内皮细胞生物学活性的变化,以及为阐明Nef参与HIV-1致病的分子机制奠定基础。方法应用本实验室已经建立保存的HIV-1Nef基因在内皮细胞的稳定表达细胞株ECV304-Nef和其阴性对照细胞株ECV304 pcDNA 3.1(+),通过RT-PCR、实时定量PCR(real-time PCR)、Western blot、FCM和细胞黏附试验分析ECV304-Nef细胞ICAM-1的表达水平。结果 RT-PCR、real-time PCR结果显示ECV304-Nef细胞ICAM-1 mRNA表达水平明显升高,为对照组的(4.3±0.2)倍;Western blot结果示ECV304-Nef细胞I-CAM-1蛋白的表达水平高于对照组;FCM分析显示ECV304-Nef细胞和对照组细胞ICAM-1阳性细胞百分率分别为(35.3±2.2)%和(12.5±0.8)%(P0.01),两组间ICAM-1表达有显著差异。细胞黏附实验观察到ECV304-Nef细胞黏附的Jurkat细胞数明显多于对照组,荧光仪定量分析结果显示ECV304-Nef细胞黏附的Jurkat细胞的荧光强度值显著高与对照组(P0.05)。结论本实验证实了HIV-1Nef基因可以上调血管内皮细胞细胞黏附分子ICAM-1的表达。     

下丘脑、垂体条件培养基对内皮细胞NOS和ICAM-1表达的影响

动脉粥样硬化(AS)早期病变的形成包括两个重要环节：一是血液中单核细胞与内皮细胞(EC)粘附，继而迁移到内皮下转变为巨噬细胞(MP)；二是MP或平滑肌细胞(SMC)摄取脂质后转变为泡沫细胞^[1]。因而，研究EC功能对AS早期防治极为重要。我们以前的工作证实：毁损弓状核可诱发AS早期病变，如内皮变性、核肿胀、内皮下层增生出现许多大小不等的空泡、     

丹参醇提取物对内皮细胞VCAM-1、ICAM-1表达的影响

众所周知,粘附分子在内皮细胞受损过程中起了重要作用,中药丹参对血栓性疾病有治疗和预防作用,对内皮细胞有保护作用,但保护机制的研究尚不充分,如对内皮细胞粘附分子的表达是否有影响,还未见文献报道。本文用丹参醇提取物作用内皮细胞后,检测血管内皮细胞粘附分子-1(VCAM-1)和细胞间粘附分子-1(ICAM-1)表达的变化,以进一步阐明丹参对内皮细胞保护作用的机制,为临床上用丹参防治心血管疾病补充理论依据。     

肠癌癌周淋巴管的结构

恶性肿瘤的浸润转移是恶性肿瘤患者的主要死亡原因,而肿瘤细胞对淋巴管的浸润与肿瘤的转移密切相关、本文运用石蜡切片ＨＥ染色和超薄切片透射电镜观察,发现癌周淋巴管存在肿瘤细胞浸润时,内皮细胞之间开放连接明显增多,癌细胞通过开放连接进入淋巴管,同时淋巴管内皮细胞发生溶解破坏。本文也运用图象分析处理技术,对内皮细胞胞质内的质膜小泡、线粒体、粗面内质网进行分析,为探讨肿瘤淋巴管的浸润转移机理提供形态学依据。     

流体切应力对血管内皮细胞粘附分子ICAM-1的影响

目的 :探讨血液流动产生的切应力对白细胞 血管内皮细胞 (VEC)相互粘附所产生的影响及其在炎症、免疫反应、动脉粥样硬化发生发展中所起的重要作用。方法 :将已汇合的人脐静脉内皮细胞玻片放于平板流动腔中 ,以层流不同切应力 0 .6、1.2、2 .4Pa剪切不同时间 (2、8、12h) ,用免疫细胞化学方法检测VEC表面ICAM 1表达 ,以显微镜下计数阳性细胞率表示。结果 :稳层流切应力能上调HUVECICAM 1表达 ,切应力是内皮细胞粘附分子表达的调节因素之一。     

淋巴管内皮细胞透明质酸受体-1在发育小鼠肾内的表达

目的:探讨淋巴管内皮细胞透明质酸受体-1(LYVE-1)在发育小鼠肾内的表达.方法:胚胎期第13～18天(E13～18)的胎鼠和出生后第4、 14和21天(P4～21)及成年小鼠的肾,行LYVE-1免疫组织化学显色.结果:LYVE-1免疫阳性淋巴管丛最早在胚胎期第14天的小鼠肾检测到,主要位于肾皮质的动脉周围.在胚胎期第15天的肾小球中最早检测到LYVE-1免疫阳性细胞,但LYVE-1免疫阳性细胞在肾小球中的数量和位置不定.结论:LYVE-1免疫阳性细胞主要位于肾动脉周围淋巴管,在肾小球中也有LYVE-1表达.     

小鼠恶性黑色素移植瘤模型的建立及其淋巴管内皮细胞透明质酸受体1的表达

目的:建立小鼠皮肤恶性黑色素移植瘤模型,探讨小鼠皮肤恶性黑色素移植瘤组织内淋巴管的生成情况。方法:体外培养B16瘤细胞,接种B16瘤细胞于C57BL/6小鼠右侧背部皮内,构建C57BL/6小鼠皮肤恶性黑色素移植瘤模型;应用H-E染色、淋巴管内皮细胞透明质酸受体1(1ymphatic vessel endothelial hyaluronan receptor-1, LYVE-1)免疫组化染色确认模型和观察肿瘤组织内淋巴管的生成情况。结果:建立了恶性黑色素移植瘤模型;LY- VE-1主要着色于正常组织和移植瘤组织中淋巴管内皮细胞的细胞膜上;恶性黑色素瘤组织中淋巴管密度明显高于正常皮肤组织。结论:构建C57BL/6小鼠皮肤恶性黑色素移植瘤模型是获得恶性黑色素瘤组织和进一步研究的有效手段;LYVE-1是特异性较高的淋巴管内皮标记物;小鼠皮肤恶性黑色素移植瘤组织中可能存在淋巴管的新生。     

LPS的直接诱导对肺微血管内皮细胞ICAM-1的表达及对PMN黏附作用影响的研究

目的探讨内素毒(Endotoxin LPS)的直接诱导作用对肺微血管内皮细胞(PMVEC)ICAM-1表达的影响及诱导发生的PMVEC对多形核中性粒细胞(PMN)黏附作用的影响。方法100ng/m l LPS刺激PMVEC 0、2、4、6、8 h或10、50、100 ng/m l LPS刺激6 h,同时检测PMVEC ICAM-1的表达(免疫细胞化学法)、PMVEC-PMN黏附率及抗ICAM-1抗体对黏附作用的影响,并进行PMVEC与PMN黏附作用的扫描电镜观察。结果LPS的直接刺激可诱导PMVEC ICAM-1的表达增加,且表现为随LPS刺激的时间、剂量增加而增加;同时LPS直接刺激也促进了PMVEC对PMN的黏附率增加,其变化在时间与方式上几乎与ICAM-1的表达增加同步。Anti-ICAM-1抗体可以显著地抑制LPS诱导的PMVEC-PMN黏附(P<0.01)。扫描电镜可以直观地显示PMVEC-PMN黏附的超微结构表现,并且首次通过这种方式观察到了“间接系链”现象的存在。结论表明细菌致病因子LPS的直接诱导可以促进PMVEC表达ICAM-1,从而为PMVEC-PMN的黏附提供物质基础,而“间接系链”的发生更扩大和巩固了黏附效果。     

淋巴管内皮细胞的生物学特性

淋巴管作为机体内流体动力学系统之一 ,对于维持组织液的平衡、淋巴细胞的再循环 ( Recirculation of lymphocyte)、蛋白质等大分子物质的转运 ,都具有非常重要的作用。近年来研究表明 :淋巴管内皮细胞具有活跃的代谢功能 ,能够生成和灭活多种生物活性物质。本文对近年来淋巴管内皮细胞的生物学特性研究综述如下。1　淋巴管内皮细胞的生物学特性1.1　血管紧张素的转化淋巴管内皮细胞中含有 A型血管紧张素 转移酶。血管紧张素转移酶分布于内皮细胞的表面 ,已被广泛用作内皮细胞的标志。血管紧张素 转移酶是一种羧基肽酶 ,能将十肽的血管紧…     

Developmental Changes of Cell Adhesion Molecule Expression in the Fetal Mouse Liver

Developmental changes of cell adhesion molecule expression, especially in nonparenchymal cells, have hardly ever been analyzed in the murine liver. The present study was undertaken to immunohistochemically examine the expression of NCAM, ICAM, VCAM, and N‐cadherin during mouse liver development and in fetal liver cell cultures. NCAM was transiently expressed in mesenchymal cells of the septum transversum and sinusoidal cells in liver development. In vitro studies demonstrated that desmin‐positive stellate cells expressed this cell adhesion molecule. NCAM expression in periportal biliary epithelial cells and connective tissue cells also coincided well with bile duct remodeling processes in the perinatal periods. Expression of ICAM and VCAM was transiently restricted to hepatoblasts, hepatocytes and hemopoietic cells in fetal stages. N‐cadherin was expressed not only in hepatoblasts and hepatocytes, but also in nonparenchymal cells such as endothelial cells, stellate cells and connective tissue cells, however the expression was weak. These results suggest that each cell adhesion molecule may play an important role during development in hepatic histogenesis, including hepatoblast/hepatocyte‐stellate cell interactions, hemopoiesis, and bile duct morphogenesis. Anat Rec 293:1698–1710, 2010. © 2010 Wiley‐Liss, Inc.     

流体切应力和Ox—LDL地内皮细胞表面ICAM—1表达的影响

目的研究动脉粥样硬化(AS)的危险因素高脂血症、流体切应力及二者共同作用对血管内皮细胞细胞间粘附分子-1(ICAM-1)表达的影响。方法以人脐静脉内皮细胞(HUVECs)为研究对象,应用免疫组化ACB方法,观测Ox-LDL、流体切应力及二者共同作用对HUVECs的粘附分子ICAM-1表达的影响。结果与对照组相比,(1)Ox-LDL显著增加HUVECs表面ICAM-1表达;(2)流体切应力使HUVECs表面ICAM-1表达增加,但ICAM-1的表达随时间依赖性增加的趋势不明显;(3)共同作用后,HUVECsICAM-1的表达较基础表达显著增加。结论Ox-LDL、流体切应力的改变及二者共同作用显著增加H-UVECs表面ICAM-1表达。     

Fimbria-Dependent Activation of Cell Adhesion Molecule Expression in Porphyromonas gingivalis-Infected Endothelial Cells

Porphyromonas gingivalis is an oral pathogen that has recently been associated with chronic inflammatory diseases such as atherosclerosis. The strength of the epidemiological associations of P. gingivalis with atherosclerosis can be increased by the demonstration that P. gingivalis can initiate and sustain growth in human vascular cells. We previously established that P. gingivalis can invade aortic, heart, and human umbilical vein endothelial cells (HUVEC), that fimbriae are required for invasion of endothelial cells, and that fimbrillin peptides can induce the expression of the chemokines interleukin 8 and monocyte chemotactic protein. In this study, we examined the expression of surface-associated cell adhesion molecules on endothelial cells in response to P. gingivalis infection by fluorescence-activated cell sorting FACS analysis and confocal microscopy. Coculture of HUVEC with P. gingivalis strain 381 or A7436 resulted in the induction in the expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and P- and E-selectins, which was maximal at 48 h postinfection. In contrast, we did not observe induction of ICAM-1, VCAM-1, or P- or E-selectin expression in HUVEC cultured with the noninvasive P. gingivalis fimA mutant DPG3 or when P. gingivalis was incubated with fimbrillin peptide-specific anti-sera prior to the addition to HUVEC. Furthermore, the addition of a peptide corresponding to the N-terminal domain of fimbrillin to HUVEC resulted in an increase in ICAM-1, VCAM-1, and P- and E-selectins, which was maximal at 48 h and similar to that observed for live P. gingivalis. Treatment of P. gingivalis-infected HUVEC with cytochalsin D, which prevented P. gingivalis invasion, also resulted in the inhibition of ICAM-1, VCAM-1, or P- and E-selectin expression. Taken together, these results indicate that active P. gingivalis invasion of HUVEC mediated via the major fimbriae stimulates surface-associated cell adhesion molecule expression. Stimulation of adhesion molecules involved in the recruitment of leukocytes to sites of inflammation by P. gingivalis may play a role in the pathogenesis of systemic inflammatory diseases associated with this microorganism, including atherosclerosis.     

Effects of Lipopolysaccharide on Endothelial Cell Adhesion Molecule Expression in Interleukin-10 Deficient Mice

Interleukin (IL)-10 is known to inhibit the production of proinflammatory cytokines by macrophages suggesting that endogenous IL-10 may act as an anti-inflammatory agent. Because endothelial cell adhesion molecules (ECAMs) play a key role in the recruitment of leukocytes into tissue in response to an inflammatory stimulus (i.e., lipopolysaccharide (LPS)) and the following cytokine production, we wished to assess the importance of IL-10 as an endogenous modulator of ECAM expression using IL-10 deficient mice. Constitutive and LPS-stimulated expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 and E-selectin were measured in wild type C57BL/6 and IL-10 deficient mice with no signs of active enterocolitis, using the dual radiolabeled monoclonal antibody technique. We found that constitutive expression of these ECAMs did not differ between IL-10 deficient and WT mice for all organs tested. However, we demonstrated larger increments in LPS-induced expression of ICAM-1 and VCAM-1 in the vasculature of the small intestine in IL-10 deficient mice compared to WT mice. These findings suggest that endogenous IL-10 does not modulate constitutive or LPS-induced expression of ECAMs in most tissues, however it does appear to play an inhibitory role in LPS-stimulated expression of ICAM-1 and VCAM-1 in the intestinal vasculature.     

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。     

血管内皮细胞生长因子VEGF与细胞黏附分子CD15在骨肉瘤中的表达及意义的研究现状

目的 探讨血管内皮细胞生长因子VEGF与细胞黏附分子CD15在骨肉瘤中的表达及意义的研究现状.方法 通过查阅大量文献,对VEGF与CD15的相关性以及两者对骨肉瘤的作用和临床治疗的研究进展做综合分析、评价.结果 VEGF与骨肉瘤的发生密切相关,但与骨肉瘤的转移尚有争论,而CD15与肿瘤的转移有密切关系.特别是已经发生转移的骨肉瘤患者中是否存在VEGF和CD15的高表达,尚待进一步证实.有可能通过针对VEGF与CD15的研究,研发出新的临床药物,以提高高度恶性的骨肉瘤患者的生存率,并对患者的预后作出有效的评估.结论 通过对VEGF和CD15进行实验研究,很有可能找到治疗骨肉瘤的新的基因治疗靶点.