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Adhesion Molecule Expression (adhesion + molecule_expression)
Kinds of Adhesion Molecule Expression Selected AbstractsRegulation of Endothelial Cell Adhesion Molecule Expression in an Experimental Model of Cerebral MalariaMICROCIRCULATION, Issue 6 2002PHILLIPE R. BAUER ABSTRACT Objective: Plasmodium falciparum malaria in humans and animal models of this disease have revealed changes in the infected host that are consistent with a systemic inflammatory response. Although it has been proposed that endothelial cell adhesion molecules (CAM) contribute to the adhesive interactions of Plasmodium -infected erythrocytes and immune cells with vascular endothelial cells, ECAM expression has not been systematically studied in Plasmodium -infected animals. Methods: In this study, the dual radiolabeled monoclonal antibody method was used to quantify the expression of different ECAMs (ICAM-1, VCAM-1, P-selectin, E-selectin) in different regional vascular beds of Plasmodium berghei ANKA-inffected mice (PbA), a well-recognized model of human cerebral malaria. The roles of T lymphocytes and certain cytokines (TNF-,, IL-12, IFN-,) in mediating the infection-induced expression of ICAM-1 and P-selectin were assessed by using relevant mutant mice. Results: Wild-type (WT) mice exhibited highly significant increases in the expression of ICAM-1, VCAM-1, and P-selectin (but not E-selectin) in all vascular beds on the 6th day of PbA infection. The PbA -induced upregulation of ICAM-1 was significantly blunted in mice that were either deficient in IFN-,, IL-12 (but not TNF1b) or T lymphocytes (Rag-1 deficiency); however, these responses were tissue specific. Conclusions: These findings indicate that vascular endothelial cells in most regional circulations assume an inflammatory phenotype and that cytokines and immune cells mediate this response in a tissue-specific manner. [source] Brain Endothelial Adhesion Molecule Expression in Experimental ColitisMICROCIRCULATION, Issue 2 2001MIQUEL SANS ABSTRACT Objectives: 1) To determine if endothelial expression of adhesion molecules involved in leukocyte recruitment is increased in the brain and other organs in four different models of experimental colitis, and 2) to investigate whether leukocyte infiltration occurs in the brain of colitic animals. Methods: Endothelial vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) expression was quantified, using the dual radiolabeled antibody technique in rats with trinitrobenzenesulfonic acid (TNBS)-induced colitis, in mice with dextran sulfate sodium (DSS)-induced colitis, in SCID mice reconstituted with CD45RBhigh T-cells, and in IL-10,/, mice. Leukocyte infiltration in the brain of TNBS-induced colitic rats was assessed by myeloperoxidase activity and immunohistochemical staining with anti-CD45 monoclonal antibody. Results: Marked upregulation of brain endothelial VCAM-1 (2- to 5.5-fold) was consistently found in colitic animals in the four models studied. Brain VCAM-1 strongly correlated with colon VCAM-1 and colon weight. By contrast, upregulation of brain ICAM-1 in colitic animals was only observed in the CD45RBhigh transfer (3-fold) and the TNBS-induced (1.5-fold models). Heart and muscle VCAM-1 and ICAM-1 were not upregulated in colitic animals in the majority of models studied. There was no leukocyte infiltration into the brain of TNBS-induced colitic rats. Conclusions: Our study demonstrates a marked and specific upregulation of endothelial VCAM-1 in the brain of colitic animals. This activation of cerebral endothelial cells was not associated with an infiltration of leukocytes into brain tissue. [source] Developmental Changes of Cell Adhesion Molecule Expression in the Fetal Mouse LiverTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 10 2010Yoshinori Sugiyama Abstract 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. [source] Neural Cell Adhesion Molecule Expression in Adenoid Cystic Carcinoma of the Head and Neck,THE LARYNGOSCOPE, Issue 6 2000James A. Hutcheson MD Abstract Objective To investigate whether there is a correlation between neural cell adhesion molecule (NCAM) expression and perineural spread in patients with adenoid cystic carcinoma of the head and neck (ACCHN). Study Design Retrospective review of medical records and immunohistochemical staining of specimens from 37 patients treated at the University of Arkansas in Little Rock from 1987 to 1997. Methods Sections from paraffin-embedded specimens were e-amined for the presence of NCAM using monoclonal anti-NCAM antibody by avidin-biotin-pero-idase immunohistochemical staining. NCAM staining was scored in each specimen and correlated with the data obtained from patient charts. Results Twenty-five of 37 specimens (68%) showed histopathological evidence of perineural spread. All 37 specimens (100%) stained positive for NCAM, regardless of perineural spread status. Conclusion Our results suggested that the use of NCAM expression as a predictor of perineural spread is highly unlikely. [source] ChemInform Abstract: Discovery of Inhibitors of Cell Adhesion Molecule Expression in Human Endothelial Cells.CHEMINFORM, Issue 28 2001Part 1. Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a "Full Text" option. The original article is trackable via the "References" option. [source] Adhesion molecule expression by bone marrow CD34-positive cells in aplastic anemia before and after immunosuppressive therapyINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 6 2003K. Kaito Summary Appropriate adhesion between bone marrow stem cells and the marrow microenvironment is necessary for hematopoiesis, since signals that promote maturation or apoptosis are transmitted from stromal cells to stem cells. In aplastic anemia (AA), interferon- , produced by stromal cells has more influence on the pathogenesis of marrow failure than interferon- , produced by lymphocytes. We evaluated the expression of cell adhesion molecules, such as very late antigen-4 (CD49d), and -5 (CD49e) or c-kit receptor (CD117), by CD34-positive bone marrow cells in patients with AA who achieved hematological complete remission after immunosuppressive therapy. Before treatment, CD34-positive cells showed markedly higher expression of CD49d and CD49e than cells from healthy controls, indicating the strong adhesion of stem cells to the bone marrow stroma. Expression of CD49d and CD49e was significantly decreased, reaching normal levels, after hematological recovery. These findings suggest that changes in adhesion molecule expression by stem cells are important in the pathology of AA. [source] Adhesion molecule expression in experimental myositisMUSCLE AND NERVE, Issue 3 2002Tomoko Ito MD Abstract Experimental allergic myositis (EAM) in Lewis rats, induced with partially purified myosin, is regarded as a model of human polymyositis. To clarify the role of adhesion molecules in the pathogenesis of EAM in Lewis rats, we investigated intramysial expressions of the intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, and the serum level of soluble ICAM-1 in EAM rats. All the EAM rat muscles had scattered inflammatory foci, as well as cell infiltration and necrosis, by week 4 after the initial immunization (i.e., day 0 after the last immunization). As compared with the control muscles, ICAM-1 and VCAM-1 were strongly expressed immunohistochemically in the endothelium of vessels in the endomysium and perimysium, and to lesser extents in the inflammatory infiltrates and on the sarcolemma of nonnecrotic muscle fibers adjacent to the inflammatory infiltrates or invaded muscle fibers. ICAM-1 in the muscle extracts and sera from EAM rats increased on each test day, as compared with extracts from the normal controls. The values peaked on day 0 after the last immunization, then gradually decreased with time. ICAM-1 elevations in the muscle extracts were correlated with the percent of sections that had inflammatory lesions (P = 0.032) and the histological scores (P = 0.005) on day 0, whereas there was no significance on days 3 and 7. These findings suggest that the adhesion molecules ICAM-1 and VCAM-1 increase in the early stage of EAM, and function in the initiation of the inflammatory process of myositis. © 2002 Wiley Periodicals, Inc. Muscle Nerve 25: 000,000, 2002 [source] Mast cell adhesion to bronchial smooth muscle in asthma specifically depends on CD51 and CD44 variant 6ALLERGY, Issue 8 2010P.-O. Girodet To cite this article: Girodet P-O, Ozier A, Trian T, Begueret H, Ousova O, Vernejoux J-M, Chanez P, Marthan R, Berger P, Tunon de Lara JM. Mast cell adhesion to bronchial smooth muscle in asthma specifically depends on CD51 and CD44 variant 6. Allergy 2010; 65: 1004,1012. Abstract Background:, Mast cells infiltrate the bronchial smooth muscle (BSM) in asthmatic patients, but the mechanism of mast cell adhesion is still unknown. The adhesion molecules CD44 (i.e. hyaluronate receptor) and CD51 (i.e. vitronectin receptor) are widely expressed and bind to many extracellular matrix (ECM) proteins. The aims of the study are (i) to identify the role of ECM in mast cell adhesion to BSM and (ii) to examine the role of CD51 and CD44 in this adhesion. Methods:, Human lung mast cells, human mast cell line (HMC-1), and BSM cells from control donors or asthmatic patients were cultured in the presence/absence of various cytokines. Mast cell,BSM interaction was assessed using 3H-thymidine-pulsed mast cells, confocal immunofluorescence, or electron microscopy. Adhesion molecules expression and collagen production on both cell types were evaluated by quantitative RT-PCR, western blot, and flow cytometry. Results:, Mast cell adhesion to BSM cells mostly involved type I collagen of the ECM. Such an adhesion was increased in normal BSM cells under inflammatory condition, whereas it was maximal in asthmatic BSM cells. Blockade of either CD51 or CD44 significantly decreased mast cell adhesion to BSM. At the molecular level, protein and the transcriptional expression of type I collagen, CD51 or CD44 remained unchanged in asthmatic BSM cells or in mast cells/BSM cells under inflammatory conditions, whereas that of CD44 variant isoform 6 (v6) was increased. Conclusions:, Mast cell,BSM cell adhesion involved collagen, CD44, and CD51, particularly under inflammatory conditions. CD44v6 expression is increased in asthmatic BSM cells. [source] n-3 polyunsaturated fatty acid supplementation, monocyte adhesion molecule expression and pro-inflammatory mediators in Type 2 diabetes mellitusDIABETIC MEDICINE, Issue 1 2001M. J. Sampson SUMMARY Aims To examine the effect of n-3 polyunsaturated fatty acid supplements on the monocyte surface expression of adhesion molecules involved in pro-atherogenic monocyte,endothelial interactions, and on pro-inflammatory mediators in Type 2 diabetes mellitus. Methods Twenty-nine subjects with Type 2 diabetes and 21 controls without diabetes were studied. Monocyte expression of leucocyte function-associated antigens 1 and 3, intercellular adhesion molecule-1, and the major histocompatibility complex class II molecule HLA-DR were measured using a laser flow cytometric method. Supplementation with 2.08 g n-3 fatty acids for 21 days was undertaken and measurements repeated. Plasma soluble adhesion molecule concentrations, plasminogen activator inhibitor-1 activity and antigen and pro-inflammatory mediators (cysteinyl leukotriene and monocyte leukotriene B4) were also measured. Results Groups did not differ in monocyte expression of adhesion molecules or HLA-DR, or in leukotriene production although plasma soluble adhesion molecule concentrations were higher in the diabetes groups (P < 0.05). n-3 fatty acid supplementation influenced neither the expression of these molecules nor plasma soluble adhesion molecule concentrations or leukotriene production. Conclusions This study does not support increased monocyte adhesion molecule expression or abnormal monocyte production of pro-inflammatory mediators as mechanisms for increased atherogenic risk in Type 2 diabetes. Cardioprotective actions of n-3 fatty acids may not be mediated through these mechanisms. [source] Learning-associated regulation of polysialylated neural cell adhesion molecule expression in the rat prefrontal cortex is region-, cell type- and paradigm-specificEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2008Judith P. F. Ter Horst Abstract The prefrontal cortex (PFC) is an interconnected set of cortical areas that function in the synthesis of a diverse range of information and production of complex behaviour. It is now clear that these frontal structures, through bidirectional excitatory communication with the hippocampal formation, also play a substantial role in long-term memory consolidation. In the hippocampus, morphological synaptic plasticity, supported by regulation of neural cell adhesion molecule (NCAM) polysialylation status, is crucial to information storage. The recent description of polysialylated neurons in the various fields of the medial PFC suggests these structures to possess a similar capacity for synaptic plasticity. Here, using double-labelling immunohistochemistry with glutamic acid decarboxylase 67, we report that the nature of NCAM polysialic acid-positive neurons in the PFC is region-specific, with a high proportion (30,50%) of a ,-aminobutyric acid (GABA)ergic phenotype in the more ventral infralimbic, orbitofrontal and insular cortices compared with just 10% in the dorsal structures of the cingulate, prelimbic and frontal cortices. Moreover, spatial learning was accompanied by activations in polysialylation expression in ventral PFC structures, while avoidance conditioning involved downregulation of this plasticity marker that was restricted to the dorsomedial PFC , the cingulate and prelimbic cortices. Thus, in contrast to other structures integrated functionally with the hippocampus, memory-associated plasticity mobilized in the PFC is region-, cell type- and task-specific. [source] Repeated restraint stress suppresses neurogenesis and induces biphasic PSA-NCAM expression in the adult rat dentate gyrusEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2003Kara Pham Abstract Chronic restraint stress has been shown to induce structural remodelling throughout the interconnected dentate gyrus-CA3 fields. To find out how this stressor affects the rate of adult hippocampal neurogenesis, we subjected rats to acute or chronic restraint stress and assessed the proliferation, survival and differentiation of newly born cells in the dentate gyrus. We also examined polysialylated neural cell adhesion molecule expression, a molecule normally expressed in immature neurons and important for morphological plasticity. The results show that acute restraint stress did not change either the proliferation of dentate gyrus precursor cells or the expression of polysialylated neural cell adhesion molecule, whereas 3 weeks of chronic restraint stress suppressed proliferation by 24% and increased polysialylated neural cell adhesion molecule expression by 40%. The study was extended for an additional 3 weeks to trace the survival and development of the cells born after the initial 3 weeks of restraint. Rats subjected to 6 weeks of daily restraint stress exhibited suppressed cell proliferation and attenuated survival of the recently born cells after the extended time course, resulting in a 47% reduction of granule cell neurogenesis. Furthermore, 6 weeks of chronic stress significantly reduced the total number of granule cells by 13% and the granule cell layer volume by 5%. Expression of polysialylated neural cell adhesion molecule followed a biphasic time course, displaying a significant up-regulation after 3 weeks of daily restraint stress that was lost after 6 weeks of stress. These studies may help us understand the basis for hippocampal shrinkage and raise questions about the ultimate reversibility of the effects of chronic stress. [source] Dual effects of NMDA receptor activation on polysialylated neural cell adhesion molecule expression during brainstem postnatal developmentEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2001Farima Bouzioukh Abstract Here we show a dual role of N -methyl- d -aspartate receptor (NMDAR) activation in controlling polysialylated neural cell adhesion molecule (PSA-NCAM) dynamic expression in the dorsal vagal complex (DVC), a gateway for many primary afferent fibres. In this structure the overall expression of PSA-NCAM decreases during the first 2 weeks after birth to persist only at synapses in the adult. Electrical stimulation of the vagal afferents causes a rapid increase of PSA-NCAM expression both in vivo and in acute slices before postnatal day (P) 14 whereas a similar stimulation induces a decrease after P15. Inhibition of NMDAR activity in vitro completely prevented these changes. These regulations depend on calmodulin activation and cGMP production at all stages. By contrast, blockade of neuronal nitric oxide synthase (nNOS) prevented these changes only after P10 in agreement with its late expression in the DVC. The pivotal role of NMDAR is also supported by the observation that chronic blockade induces a dramatic decrease in PSA-NCAM expression. [source] Agonists of proteinase-activated receptor-2 affect transendothelial migration and apoptosis of human neutrophilsEXPERIMENTAL DERMATOLOGY, Issue 10 2007Victoria M. Shpacovitch Abstract:, Skin is the first barrier preventing microorganism invasion in host. Wounds destroy this defense barrier and, without an appropriate care, may lead to sepsis. Neutrophil activation and immigration plays an important role at the inflammatory stage of wound healing. Neutrophils are known to express proteinase-activated receptors (PARs), which can be activated by serine proteases, also by enzymes involved in wound healing. We previously reported that PAR2 agonists up-regulate cell adhesion molecule expression and cytokine production by human neutrophils. Here, we demonstrate that PAR2 agonists (serine proteases as well as synthetic peptides) reduce transendothelial migration of neutrophils and prolong their life in vitro. Synthetic PAR2 agonist also enhanced protective interferon (IFN),-induced Fc,RI expression at neutrophil cell surface. Of note, IFN, is a cytokine, which was used in clinical trials to reactivate human neutrophil functions during sepsis. Moreover, we observed a significant increase of PAR2 expression on cell surface of neutrophils from septic patients as compared with healthy volunteers. Together, our results indicate that PAR2 may be involved in the pathophysiology of neutrophil-endothelial interactions during wound healing or later during sepsis in humans, potentially by affecting neutrophil apoptosis, transendothelial migration and Fc, receptor-mediated phagocytosis. [source] Neural cell adhesion molecule expression: No correlation with perineural invasion in cutaneous squamous cell carcinoma of the head and neckHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 6 2009C. Arturo Solares MD Abstract Background. Perineural invasion (PNI) in cutaneous squamous cell carcinoma of the head and neck (CSCCHN) is associated with decreased survival, particularly in patients with clinical signs of cranial nerve involvement. There is evidence to indicate that neural cell adhesion molecule (N-CAM) confers capability of PNI. We analyzed our own patient population to determine if N-CAM predicted clinical PNI in CSCCHN. Methods. Tissue from patients with CSCCHN and clinical PNI, who underwent surgery between 1998 and 2005, was immunostained for N-CAM. In addition, non-PNI CSCCHN and normal nerve sections were also stained. A section of neuroendocrine tumor was included in each slide as a positive control. In addition, most of the sections also had an "inbuilt control" in the CD56 positive natural killer T cells that formed part of the inflammatory reaction to the tumors. Results. Tissue was available from 14 patients with CSCCHN and clinical PNI. The analysis was carried out in 14 patients without PNI and 4 normal nerves. N-CAM was not expressed in any of our PNI CSCCHN specimens or non-PNI controls. It was strongly expressed in the neuroendocrine tumors and positive in-built controls, as well as in normal nerve tissue. Conclusion. N-CAM expression did not predict neurotropism in our patient population. Additional studies are required to identify the cell surface markers expressed by CSCCHN which confer neurotropism capabilities. © 2009 Wiley Periodicals, Inc. Head Neck, 2009 [source] Pathogenesis of Helicobacter pylori InfectionHELICOBACTER, Issue 2006Masanori Hatakeyama Abstract Much interest has been shown in the relationship between Helicobacter pylori infection and gastric carcinogenesis. It is becoming clearer that H. pylori strains carrying a functional cag pathogenicity island (cagPAI), which encodes the type IV secretion system (TFSS) and its effector CagA, play an important role in the development of gastric carcinoma. Furthermore, genetic polymorphism present in the cagA gene appears to influence the degree of an individual cagPAI-positive H. pylori to elicit gastric mucosal lesions, and this process is significantly affected by host genetic polymorphisms such as proinflammatory cytokine gene polymorphisms. Pathomechanism of gastric carcinogenesis associated with H. pylori includes bacteria,host interaction leading to morphologic alterations such as atrophic gastritis and gastrointestinal metaplasia mediated by COX-2 overexpression, cancer cell invasion, and neo-angiogenesis via TLR2/TLR9 system and transcription factors (e.g., NF-,B) activation. In addition, H. pylori infection triggers adhesion molecule expression and activity and produces an enhancement in oxidative stress interacting with gastric production of appetite hormone ghrelin and nonsteroidal anti-inflammatory drugs. [source] Expression of VCAM-1, ICAM-1, E- and P-selectin and tumour-associated macrophages in renal cell carcinomaHISTOPATHOLOGY, Issue 1 2000B Hemmerlein Aims Neoangiogenesis is accompanied by an increase in endothelial surface, which can support infiltration by immune cells depending on adhesion molecule expression. Therefore, the expression of cell adhesion molecules on microvessels and epithelial cells was analysed in renal cell carcinomas as compared to tumour-free tissue. Methods and results PECAM-1, CD34, ICAM-1, VCAM-1, VLA-4, P- and E-selectin, the macrophage antigens Ki-M1P and Mac-1, and lymphocyte function antigen LFA-1 were identified immunohistochemically. VCAM-1, ICAM-1, and E-selectin were equally or less expressed, whereas P-selectin was increased on microvessels in tumour tissue. The density of VCAM-1-positive tumour microvessels correlated positively with an advanced tumour stage and E- and P-selectin-positive tumour microvessels with the amount of associated macrophages. The expression of ICAM-1 and VCAM-1 on neoplastic epithelia correlated with an increased density of macrophages and a minor degree of tumour differentiation. Conclusions The positive correlation of macrophage infiltration and expression of cell adhesion molecules on tumour microvessels and epithelia with minor tumour differentiation and an advanced stage indicates that adhesion molecule expression is not associated with an effective antitumour function of macrophages [source] Down-regulation of endothelial adhesion molecules and leukocyte adhesion by treatment with superoxide dismutase is beneficial in chronic immune experimental colitisINFLAMMATORY BOWEL DISEASES, Issue 10 2005Joaquim Seguí PhD Abstract Modulation of adhesion molecule expression that govern trafficking of leukocytes into the inflamed intestine is envisioned as a new strategy for treatment of inflammatory bowel disease (IBD). This study was designed to determine the impact of reducing oxidative stress on adhesion molecules expression and leukocyte recruitment in experimental chronic colitis. For that purpose, colitic interleukin-10 knockout and wild-type mice were studied. Groups of animals were treated with Cu/Zn superoxide dismutase (SOD1) 13 mg/kg/d or vehicle for either 7 or 14 days. Expression of vascular cell adhesion molecule-1 and mucosal addressin cell adhesion molecule-1 were determined; leukocyte-endothelial cell interactions in colonic venules were studied with intravital microscopy; and changes in colon pathology and biomarkers of colitis severity were determined. Development of colitis was associated with a marked increase in endothelial vascular cell adhesion molecule-1 and mucosal addressin cell adhesion molecule-1 expression, which were significantly reduced by treatment with SOD1. The increase in leukocyte rolling and adhesion in colonic venules of colitic mice were significantly reduced by administration of SOD1. This treatment markedly reduced colonic lipid hydroperoxidation, myeoloperoxidase activity, and plasma levels of serum amyloid A protein and resulted in significant, although modest, reductions in histologic damage score. The therapeutic value of SOD1 when administered prophylactically was assessed in the dextran sulfate sodium model of colitis with similar positive results. These results indicate that SOD1 affords significant amelioration of colonic inflammatory changes in experimental colitis. Down-regulation of adhesion molecule expression, reduction of lipid hydroperoxidation, and recruitment of leukocytes into the inflamed intestine contribute to this beneficial effect. [source] Adhesion molecule expression by bone marrow CD34-positive cells in aplastic anemia before and after immunosuppressive therapyINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 6 2003K. Kaito Summary Appropriate adhesion between bone marrow stem cells and the marrow microenvironment is necessary for hematopoiesis, since signals that promote maturation or apoptosis are transmitted from stromal cells to stem cells. In aplastic anemia (AA), interferon- , produced by stromal cells has more influence on the pathogenesis of marrow failure than interferon- , produced by lymphocytes. We evaluated the expression of cell adhesion molecules, such as very late antigen-4 (CD49d), and -5 (CD49e) or c-kit receptor (CD117), by CD34-positive bone marrow cells in patients with AA who achieved hematological complete remission after immunosuppressive therapy. Before treatment, CD34-positive cells showed markedly higher expression of CD49d and CD49e than cells from healthy controls, indicating the strong adhesion of stem cells to the bone marrow stroma. Expression of CD49d and CD49e was significantly decreased, reaching normal levels, after hematological recovery. These findings suggest that changes in adhesion molecule expression by stem cells are important in the pathology of AA. [source] Expression of VCAM-1, ICAM-1, E-selectin, and P-selectin on endothelium in situ in patients with erythroderma, mycosis fungoides and atopic dermatitisJOURNAL OF CUTANEOUS PATHOLOGY, Issue 9 2000Vigfús Sigurdsson Background: Erythroderma may result from different causes. At present it is unclear whether the patho-mechanisms that lead to these different types of erythroderma are identical or different. Adhesion molecules and their ligands play a major role in endothelial-leukocyte interactions, which affect the binding, transmigration and infiltration of lymphocytes and mononuclear cells during inflammation, injury, or immunological stimulation. The aim of this study was to investigate the adhesion molecule expression on endothelial cells in erythroderma in situ. Methods: Snap-frozen skin biopsy specimens from 23 patients with erythroderma were studied. Eight had idiopathic erythroderma, 5 erythrodermic atopic dermatitis, 4 Sézary syndrome and 6 had erythroderma from miscellaneous causes. As a control we studied skin specimens from 10 patients with mycosis fungoides, 5 patients with atopic dermatitis and 5 healthy non-atopic volunteers. To determine adhesion molecule expression on endothelial cells in situ, sections were immuno-histochemically double stained with biotinylated Ulex Europaeus agglutinin 1 as a pan-endothelial cell marker, and for the adhesion molecules VCAM-1, ICAM-1, E-, and P-selectin. All double- and single-stained blood vessels in the dermis were counted. Results: Mean endothelial expression in erythroderma was as follows: VCAM-1 51.4%, ICAM-1 70.1%, E-selectin 43.5%, and P-selectin 52.6%. There was no statistical difference between different groups of erythroderma. Mean expression of all adhesion molecules tested, was in Sézary syndrome higher than in mycosis fungoides albeit not significant. In erythrodermic atopic dermatitis only VCAM-1 expression was significantly higher than in lesional skin of atopic dermatitis. No differences were observed in expression of the other three adhesion molecules. Conclusions: There is no difference regarding adhesion molecule expression on endothelial cells between different types of erythroderma. [source] The effect of butyric acid on adhesion molecule expression by human gingival epithelial cellsJOURNAL OF PERIODONTAL RESEARCH, Issue 4 2008S. Takigawa Background and Objective:, Short-chain fatty acids, such as butyric acid, are detected in periodontal pockets and are thought to be involved in the initiation and progression of periodontal disease. In the present study, we examined the effects of butyric acid on adhesion molecule expression by human gingival epithelial cells. Material and methods:, The human gingival carcinoma cell line, Ca9-22, was cultured in media that contained different concentrations of butyric acid. Results:, Cell numbers were significantly decreased in a dose-dependent manner by butyric acid at concentrations of , 0.2 mm. The expression of intercellular adhesion molecule-1 mRNA was significantly increased 6 h after stimulation. By contrast, the expression levels of integrins ,6 and ,4 were decreased. Similar results were obtained by flow cytometry. Conclusion:, The results of the present study indicate that butyric acid alters the expression of adhesion molecules by Ca9-22 cells. The elucidation of the mechanism of action of butyric acid on the periodontium may help to clarify several aspects of the onset and progression of periodontal disease. [source] Platelet function in sepsisJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 12 2004A. YAGUCHI Summary.,Background: Coagulation abnormalities and thrombocytopenia are common in severe sepsis, but sepsis-related alterations in platelet function are ill-defined. Objectives: The purpose of this study was to elucidate the effect of sepsis on platelet aggregation, adhesiveness, and growth factor release. Patients and methods: Agonist-induced platelet aggregation was measured in platelet-rich plasma separated from blood samples collected from 47 critically ill patients with sepsis of recent onset. Expression of platelet adhesion molecules was measured by flow cytometry and the release of vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) was measured by ELISA in the supernatant of platelet aggregation. Results: Septic patients had consistently decreased platelet aggregation compared with controls, regardless of the platelet count, thrombin generation, or overt disseminated intravascular coagulation (DIC) status. The severity of sepsis correlated to the platelet aggregation defect. Adhesion molecules, receptor expression (CD42a, CD42b, CD36, CD29, PAR-1), and ,-granule secretion detected by P-selectin expression remained unchanged but the release of growth factors was differentially regulated with increased VEGF and unchanged PDGF after agonist activation even in uncomplicated sepsis. Conclusions: Sepsis decreases circulating platelets' hemostatic function, maintains adhesion molecule expression and secretion capability, and modulates growth factor production. These results suggest that sepsis alters the hemostatic function of the platelets and increases VEGF release in a thrombin-independent manner. [source] Aspirin inhibits endothelial cell activation induced by antiphospholipid antibodiesJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 7 2004S. Dunoyer-Geindre Summary., Background : Antiphospholipid antibodies (APLA) have been shown to activate endothelial cells (EC) in vitro, as documented by an increased expression of tissue factor as well as leukocyte adhesion molecules such as intercellular adhesion molecule-1, vascular cell adhesion molecule (VCAM)-1 and E-selectin. Currently, treatment of patients with the antiphospholipid syndrome includes aspirin, particularly for women with recurrent fetal loss. Objective : The present study was undertaken to investigate whether aspirin interferes with EC activation induced by APLA in vitro. Methods : IgG from 14 patients with APLA, and suffering from thrombotic complications and/or pregnancy morbidity, and control IgG were tested for their ability to modify the expression of VCAM-1 in human umbilical vein endothelial cells. VCAM-1 antigen was measured by flow cytometry and its mRNA by quantitative reverse transcriptase-polymerase chain reaction. Results : Incubation of EC with IgG from most of the patients led to a higher VCAM-1 expression compared with incubation with control IgG. The effect of aspirin was studied for the eight IgG samples that induced a more than 50% increase in VCAM-1. Aspirin (10 mm) treatment of the cells significantly reduced the VCAM-1 response to these APLA. Conclusions : Our results indicate that besides its antiplatelet properties, aspirin exerts a protective effect towards APLA at the EC level by decreasing leukocyte adhesion molecule expression at the cell surface. [source] Independence of tumor necrosis factor-,-induced adhesion molecule expression from sphingosine 1-phosphate signaling in vascular endothelial cellsJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 6 2004Y. Miura No abstract is available for this article. [source] Effects of statins on adhesion molecule expression in endothelial cellsJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 11 2003Y. Dimitrova Summary.,Background:,Inhibitors of HMG-CoA reductase are widely used to prevent atherosclerosis progression. The expression of adhesion molecules on activated endothelial cells (EC) is an important step in the initiation and progression of atherosclerosis. Objectives:,We investigated whether adhesion molecule expression on activated EC is influenced by simvastatin, fluvastatin and pravastatin and, if so, by which mechanisms. Methods:,Human EC from umbilical veins or saphenous veins were pretreated overnight with statins with or without mevalonate, and also for simvastatin or fluvastatin with the isoprenoid intermediates, farnesyl pyrophosphate (FPP), or geranylgeranyl pyrophosphate (GGPP). After 4,6 h activation with tumor necrosis factor (TNF)-, or lipopolysaccharide (LPS), surface adhesion molecule expression was evaluated by ELISA and by flow cytometry. The same experiments were performed with selective inhibitors of geranylgeranyltransferase (GGTI-286) and farnesyltransferase (FTI-277). Results:,Pretreatment with simvastatin, fluvastatin or pravastatin potentiated the TNF-, and LPS-induced expression of E-selectin and VCAM-1, and mevalonate reversed the potentiating effect of these statins. GGPP also reversed the potentiating effect of simvastatin or fluvastatin on adhesion molecule expression, while FPP only partially reversed this effect. Furthermore, GGTI-286, but not FTI-277, mimicked the effect of simvastatin by increasing the TNF-,-mediated overexpression of E-selectin. Conclusions:,Statins increase E-selectin- and VCAM-1-induced expression on vascular endothelial cells stimulated with TNF-, or LPS. The inhibition of geranylgeranylated proteins could contribute to this effect. [source] In vitro study examining the effect of sub-lethal QS 755 nm lasers on the expression of p16INK4a on melanoma cell linesLASERS IN SURGERY AND MEDICINE, Issue 2 2003Henry H.L. Chan Abstract Background and Objectives Q-switched lasers had been used in the treatment of lentigo maligna but their role remains controversial. While previous studies have addressed the change in adhesion molecule expression after sub-lethal laser damage, no study has addressed the impact of sub-lethal laser damage at a molecular level. The p16 gene has been proposed as the candidate gene for melanoma. Our objective is to examine the effect of sub-lethal laser damage on p16 expression in melanoma cell lines. Study Design/Materials and Methods Three human melanoma cell lines,HTB 66, Sk-mel-24 (HTB 71), and G361,were irradiated by a Q-switched 755 nm Alexandrite laser at fluencies that ranged from 0.85 to 2.0 J/cm2. HTB 66 was the only cell line with significant expression of p16INK4a while the other two cells lines were p16INK4a negative and served as negative control. Protein and mRNA expression for p16 were assessed by flow cytometry and RT-PCR, respectively. Results The level of p16INK4a protein in cell line HTB 66 increased significantly after laser irradiation as compared with non-irradiated cells. The level of p16INK4a protein did not change in p16INK4a-negative cell lines (Sk-mel-24 and G361). However, there was only a slight increase in the percentage of G0/G1 phase cells. Conclusions Sub-lethal laser damage could increase DNA damage leading to an increase in p16 expression, and such effect would be particularly undesirable for patients with p16 mutation. Further studies are warranted to examine the role of sub-lethal laser damage in inducing p16 mutation. Lasers Surg. Med. 32:88,93, 2003. © 2003 Wiley-Liss, Inc. [source] Effect of isoflurane on monocyte adhesion molecule expression in human whole blood,ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2003L. W. De Rossi Background: Recruitment of monocytes to inflamed tissue is a crucial step in the acute inflammatory reaction. Adherence of monocytes to endothelial cells followed by transmigration depends on monocyte surface adhesion molecules, inflammatory cytokines and chemoattractant chemokines. In the present study, we determined the effect of isoflurane on monocyte adhesion receptor expression in vitro. Methods: Citrated whole blood was incubated for 60 min with either 0.5 or 1 MAC isoflurane. In unstimulated blood samples and after stimulation with N-formyl-methionyl-leucyl-phenylalanine (FMLP) monocyte cell-surface expression of the selectins PSGL-1 and L-selectin, and the ,2 -integrins CD11a and CD11b were evaluated by flow cytometry. Results: Isoflurane reduced significantly the expression of PSGL-1 on unstimulated monocytes, whereas the remaining selectins and ,2 -integrins were not affected. At both concentrations, the FMLP-induced removal of PSGL-1 from the monocyte surface was increased. Furthermore, at 1 MAC isoflurane the FMLP-induced increase in CD11a expression was significantly inhibited. The surface expression of L-selectin and CD11b was not affected following exposure to isoflurane. Conclusion: Isoflurane increases the removal of the selectin PSGL-1 from the monocyte surface. Since PSGL-1 is important during the initial step of monocyte adhesion to endothelial P-selectin, the decrease in monocyte surface PSGL-1 may have profound effects on monocyte,endothelial interactions. Furthermore, the effects of isoflurane on monocyte adhesion molecule expression are different from those reported for neutrophils. [source] Developmental Changes of Cell Adhesion Molecule Expression in the Fetal Mouse LiverTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 10 2010Yoshinori Sugiyama Abstract 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. [source] The Role of Amniotic Fluid Interleukin-6, and Cell Adhesion Molecules, Intercellular Adhesion Molecule-1 and Leukocyte Adhesion Molecule-1, in Intra-Amniotic InfectionAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2000CHAUR-DONG HSU 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. [source] Outer membrane vesicles from Neisseria meningitidisAPMIS, Issue 3 2002Effects on leukocyte adhesion molecules, reactive oxygen species Flow cytometry was used to study the expression of leukocyte adhesion molecules CD11a, CD11b, CD11c, CD14, and CD62L (L-selectin) and production of reactive oxygen species (ROS) in an ex vivo human whole-blood system stimulated with lipopolysaccharide-containing outer membrane vesicles (LPS-OMV) from N. meningitidis. Results demonstrated a dose-dependent increase in surface expression of CD11a, CD11b, CD11c and CD14 in granulocytes and monocytes (maximal at 30,120 min) upon OMV-LPS challenge, whereas CD62L expression was heavily downregulated (maximal at 30,120 min). The OMV-associated LPS was almost as potent (on a weight basis) as purified LPS from E. coli in inducing adhesion molecule modulation but the response was delayed. Upon stimulation with OMV-LPS or E. coli -LPS, the production of intracellular ROS increased in both granulocytes and monocytes when dihydroethidium (DHE, mainly reflecting superoxide anion) was used as a probe, whereas peroxynitrite production monitored with dihydrorhodamine 123 (DHR) was not significantly changed. The OMV-mediated modulation of leukocyte adhesion molecule expression and increased ROS production may certainly lead to increased entrapment of leukocytes in the microcirculation and contribute to untoward inflammatory reactions as seen in systemic meningococcal disease. [source] Effects of a 50 Hz sinusoidal magnetic field on cell adhesion molecule expression in two human osteosarcoma cell lines (MG-63 and Saos-2)BIOELECTROMAGNETICS, Issue 5 2003Maria Teresa Santini Abstract The possibility that a sinusoidal 50 Hz magnetic field with a magnetic flux density of 0.5 mT can induce variations in the expression of cell adhesion molecules (CAMs) in two human osteosarcoma cell lines (MG-63 and Saos-2) was investigated. In particular, the expression of two important integrins, VLA-2, the receptor for collagen, and VLA-5, the receptor for fibronectin, as well as CD44, were examined in both cell lines after these had been exposed for 7 and 14 days to a 50 Hz, 0.5 mT field. Cell surface morphology (scanning electron microscopy), cell growth characteristics (growth curves and cell cycle phase distribution), and cell death (necrosis and apoptosis) were also examined. The results demonstrate that no variations in surface morphology and cell death occurred between control and exposed cells in both MG-63 and Saos-2 cells, while significant changes were noted in cell growth and fibronectin and CD44 expression in MG-63 cells. The results are discussed in view of the important role that CAMs play in controlling various cancer cell functions, particularly proliferation and metastasis. Bioelectromagnetics 24:327-338, 2003. © 2003 Wiley-Liss, Inc. [source] | ||||||||||||||||||||||||||||