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Variety Of Cells (variety + of_cell)
Terms modified by Variety Of Cells Selected AbstractsThe CD200 and CD200 receptor cell surface proteins interact through their N-terminal immunoglobulin-like domainsEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 6 2004Deborah Hatherley Abstract CD200 (OX2) is a broadly distributed cell surface glycoprotein that interacts with a receptor on myeloid cells (CD200R) involved in regulation of macrophage function. Both CD200 and CD200R contain two Ig superfamily domains like many other leukocyte membrane proteins. Site-directed mutagenesis of CD200R showed that, like CD200, it interacted through its N-terminal domain. This indicated that the cell-cell interaction spans four Ig superfamily domains and this distance is similar to many interactions found between T,cells and antigen-presenting cells. This suggests that this topology is also important in interactions of CD200 on a variety of cells with CD200R on myeloid cells, and comparable contact sites may be important mediating regulation in other cell-cell interactions. The mutagenesis showed that the binding involved the predicted GFCC, face of its N-terminal domain, like that of CD200, suggesting that the interaction evolved from a homotypic interaction. [source] Bumetanide, the Specific Inhibitor of Na+ -K+ -2Cl, Cotransport, Inhibits 1,,25-Dihydroxyvitamin D3 -Induced Osteoclastogenesis in a Mouse co-culture SystemEXPERIMENTAL PHYSIOLOGY, Issue 5 2003Hyun-A Lee The Na+ -K+ -2Cl, cotransporter (NKCC1) is responsible for ion transport across the secretory and absorptive epithelia, the regulation of cell volume, and possibly the modulation of cell growth and development. It has been reported that a variety of cells, including osteoblasts, contain this cotransporter. In this study, the physiological role of NKCC1 in osteoclastogenesis was exploited in a co-culture system. Bumetanide, a specific inhibitor of NKCC1, reduced the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. In order to investigate the mechanism by which bumetanide inhibits osteoclastogenesis, the mRNA expressions of the receptor activator of nuclear factor (NF)-,B ligand (RANKL) and osteoprotegerin (OPG) were analysed by RT-PCR. Exposure of osteoblastic cells to a medium containing 1 µM bumetanide reduced RANKL mRNA expression induced by 10 nM 1,,25-dihydroxyvitamin D3 (1,,25(OH)2D3, in a dose-dependent manner. In addition, RANKL expression was also analysed with enzyme-linked immunosorbant assay (ELISA) using anti-RANKL antibody. The expression of RANKL was decreased with the increase of bumetanide concentration. In contrast, the expression of OPG mRNA, a novel tumour necrosis factor (TNF) receptor family member was increased in the presence of bumetanide. These results imply that bumetanide inhibits osteoclast differentiation by reducing the RANKL/OPG ratio in osteoblastic cells. However, no significant difference in M-CSF mRNA expression was observed when bumetanide was added. Also, we found that the phosphorylation of c-Jun NH2 -terminal kinase (JNK), which regulates the activity of various transcriptional factors, was reduced by bumetanide treatment. Conclusively, these findings suggest that NKCC1 in osteoblasts has a pivotal role in 1,,25(OH)2D3 -induced osteoclastogenesis partly via the phosphorylation of JNK. [source] Various cells of the immune system and intestine differ in their capacity to reduce hexavalent chromiumFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2003Richa Shrivastava Abstract The cells of the immune system form a strong line of defence against foreign substances. The present study was undertaken to investigate the capacity of different cells of Wistar rats to reduce potentially carcinogenic hexavalent chromium (Cr-VI) into less toxic trivalent chromium in vitro. 5×106 cells were incubated with 10 or 25 ,g ml,1 of Cr (VI) in the form of K2Cr2O7 at 37°C in the presence of 5% CO2 in air. At various time periods the remaining amount of Cr (VI) was measured and the percentage of Cr (VI) reduced was calculated. Among the single cell suspensions from the splenic cells a peak reduction of 55% was observed with the total spleen cells, 40% with the B-lymphocyte-enriched subpopulation, 10% with T-lymphocytes and 24% with the macrophages. The reduction by splenic and peritoneal macrophages was similar. Total thymocytes reduced 54% of the Cr (VI). Since the most common route of entry of chromium is through drinking water and food, intestinal cells were also investigated. Among the intestinal cells the maximum reduction of 100% (of 10 ,g ml,1) was observed with the upper villus cells and 72% with the middle villus cells while reduction was the least (4%) with the crypt cells. The reduction in the intestinal loop in situ was 100%. The time taken by each cell type for the peak reduction to Cr (VI) was markedly different. The findings thus show that the capacity of different cells in the body differs vastly in their capacity and time taken to reduce hexavalent chromium. The most efficient handling of Cr (VI) by the intestine, due to the presence of a variety of cells and bacteria, protects the body from its adverse effects. [source] Integrin signaling through FAK in the regulation of mammary stem cells and breast cancerIUBMB LIFE, Issue 4 2010Jun-Lin Guan Abstract Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase identified as a key mediator of intracellular signaling by integrins, a major family of cell surface receptors for extracellular matrix, in the regulation of different cellular functions in a variety of cells. Upon activation by integrins through disruption of an autoinhibitory mechanism, FAK undergoes autophosphorylation and forms a complex with Src and other cellular proteins to trigger downstream signaling through its kinase activity or scaffolding function. A number of integrins are identified as surface markers for mammary stem cells (MaSCs), and both integrins and FAK are found to play crucial roles in the maintenance of MaSCs in studies using mouse models, suggesting that integrin signaling through FAK may serve as a functional marker for MaSCs. Consistent with previous studies linking increased expression and activation of FAK to human breast cancer, these findings suggest a novel cellular mechanism of FAK promotion of mammary tumorigenesis by maintaining the pools of MaSCs as targets of oncogenic transformation. Furthermore, FAK inactivation in mouse models of breast cancer also reduced the pool of mammary cancer stem cells (MaCSCs), decreased their self-renewal in vitro, and compromised their tumorigenicity and maintenance in vivo, suggesting a potential role of integrin signaling through FAK in breast cancer growth and progression through its functions in MaCSCs. This review discusses these recent advances and future studies into the mechanism of integrin signaling through FAK in breast cancer through regulation of MaCSCs that may lead to development of novel therapies for this deadly disease. © 2010 IUBMB IUBMB Life, 62(4): 268,276, 2010 [source] Role of the metastasis-promoting protein osteopontin in the tumour microenvironmentJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 8 2010Pieter H. Anborgh Abstract Osteopontin (OPN) is a secreted protein present in bodily fluids and tissues. It is subject to multiple post-translational modifications, including phosphorylation, glycosylation, proteolytic cleavage and crosslinking by transglutamination. Binding of OPN to integrin and CD44 receptors regulates signalling cascades that affect processes such as adhesion, migration, invasion, chemotaxis and cell survival. A variety of cells and tissues express OPN, including bone, vasculature, kidney, inflammatory cells and numerous secretory epithelia. Normal physiological roles include regulation of immune functions, vascular remodelling, wound repair and developmental processes. OPN also is expressed in many cancers, and elevated levels in patients' tumour tissue and blood are associated with poor prognosis. Tumour growth is regulated by interactions between tumour cells and their tissue microenvironment. Within a tumour mass, OPN can be expressed by both tumour cells and cellular components of the tumour microenvironment, and both tumour and normal cells may have receptors able to bind to OPN. OPN can also be found as a component of the extracellular matrix. The functional roles of OPN in a tumour are thus complex, with OPN secreted by both tumour cells and cells in the tumour microenvironment, both of which can in turn respond to OPN. Much remains to be learned about the cross-talk between normal and tumour cells within a tumour, and the role of multiple forms of OPN in these interactions. Understanding OPN-mediated interactions within a tumour will be important for the development of therapeutic strategies to target OPN. [source] Stem cells and pulmonary metamorphosis: New concepts in repair and regenerationJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2005Jason M. Aliotta Adult stem cells are likely to have much more versatile differentiation capabilities than once believed. Numerous studies have appeared over the past decade demonstrating the ability of adult stem cells to differentiate into a variety of cells from non-hematopoietic organs, including the lung. The goal of this review is to provide an overview of the growth factors which are thought to be involved in lung development and disease, describe the cells within the lung that are believed to replace cells that have been injured, review the studies that have demonstrated the transformation of bone marrow-derived stem cells into lung cells, and describe potential clinical applications with respect to human pulmonary disease. © 2005 Wiley-Liss, Inc. [source] Macrophage migration inhibitor factor (MIF) can induce oxidative injury and apoptotic cell death of spinal cord neuronsJOURNAL OF NEUROCHEMISTRY, Issue 2003M. Toborek MIF is a cytokine produced by a variety of cells and tissues including the CNS. It can exert a variety of biological functions, such as induction of inflammatory responses and counterregulation of glucocorticoid effects. However, the role of MIF in the pathogenesis of spinal cord trauma is not fully understood. Therefore, the aim of the present study was to evaluate the cellular effects of MIF in cultured spinal cord neurons. A 3-h exposure to MIF significantly enhanced intracellular calcium levels; an effect which was prevented by TMB-8, an antagonist of the IP3 receptor. In addition, MIF treatment increased oxidative stress, decreased viability of spinal cord neurons, increased LDH release and stimulated apoptosis. These results suggest that MIF may play an important role in secondary spinal cord injury. Acknowledgements:, Supported by grants from KSCHIRT and Philip Morris External Research Program. [source] Comparative proteomics of human embryonic stem cells and embryonal carcinoma cellsPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 7 2010Raghothama Chaerkady Abstract Pluripotent human embryonic stem cells (ESCs) can be differentiated in vitro into a variety of cells which hold promise for transplantation therapy. Human embryonal carcinoma cells (ECCs), stem cells of human teratocarcinomas, are considered a close but malignant counterpart to human ESCs. In this study, a comprehensive quantitative proteomic analysis of ESCs and ECCs was carried out using the iTRAQ method. Using two-dimensional LC and MS/MS analyses, we identified and quantitated ,1800 proteins. Among these are proteins associated with pluripotency and development as well as tight junction signaling and TGF, receptor pathway. Nearly ,200 proteins exhibit more than twofold difference in abundance between ESCs and ECCs. Examples of early developmental markers high in ESCs include ,-galactoside-binding lectin, undifferentiated embryonic cell transcription factor-1, DNA cytosine methyltransferase 3, isoform-B, melanoma antigen family-A4, and interferon-induced transmembrane protein-1. In contrast, CD99-antigen (CD99), growth differentiation factor-3, cellular retinoic acid binding protein-2, and developmental pluripotency associated-4 were among the highly expressed proteins in ECCs. Several proteins that were highly expressed in ECCs such as heat shock 27,kDa protein-1, mitogen-activated protein kinase kinase-1, nuclear factor of , light polypeptide gene enhancer in B-cells inhibitor like-2, and S100 calcium-binding protein-A4 have also been attributed to malignancy in other systems. Importantly, immunocytochemistry was used to validate the proteomic analyses for a subset of the proteins. In summary, this is the first large-scale quantitative proteomic study of human ESCs and ECCs, which provides critical information about the regulators of these two closely related, but developmentally distinct, stem cells. [source] Lung cancer A549 cells migrate directionally in DC electric fields with polarized and activated EGFRsBIOELECTROMAGNETICS, Issue 1 2009Xiaolong Yan Abstract Endogenous direct-current electric fields (dcEFs) occur in vivo in the form of epithelial transcellular potentials or neuronal field potentials. A variety of cells respond to dcEFs by migrating directionally, and this is termed galvanotaxis. The mechanism by which dcEFs direct cell movement, however, is not yet understood, and the effects on lung cancer cells are entirely unknown. We demonstrated that cultured human lung adenocarcinoma A549 cells migrate toward the cathode in applied dcEFs at 3 V/cm. Fluorescence microscopy showed that both epidermal growth factor receptors (EGFRs) and F-actin are polarized to the cathode. EGFR inhibitors, cetuximab and AG1478, reduced the migration rate and directed motility in dcEFs. Western blots showed that ERK and AKT signaling pathways were prominently promoted by dcEFs. EGFR inhibitors could reduce this promotion but not completely. These data suggest that polarization of EGFRs and the activation of their downstream signals play an important role in the galvanotaxis of A549 cells in dcEFs. Bioelectromagnetics 30:29,35, 2009. © 2008 Wiley-Liss, Inc. [source] Pentraxins: Multifunctional proteins at the interface of innate immunity and inflammationBIOFACTORS, Issue 2 2009Livija Deban Abstract Pentraxins are a family of multimeric pattern recognition proteins highly conserved in evolution. On the basis of the primary structure of the protomer, pentraxins are divided into two groups: short pentraxins and long pentraxins. C reactive protein, the first pattern recognition receptor identified, and serum amyloid P component are classic short pentraxins produced in the liver in response to IL-6. Long pentraxins, including the prototype PTX3, are expressed in a variety of tissues. PTX3 is produced by a variety of cells and tissues, most notably dendritic cells and macrophages, in response to Toll-like receptor (TLR) engagement and inflammatory cytokines. Through interaction with several ligands, including selected pathogens and apoptotic cells, pentraxins play a role in complement activation, pathogen recognition and apoptotic cell clearance. In addition, PTX3 is involved in the deposition of extracellular matrix and female fertility. Unlike the classic short pentraxins CRP and SAP, PTX3 primary sequence and regulation are highly conserved in man and mouse. Thus, gene targeting identified PTX3 (and presumably other members of the family) as multifunctional soluble pattern recognition receptors acting as a nonredundant component of the humoral arm of innate immunity and involved in tuning inflammation, matrix deposition, and female fertility. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Efficient expression and purification of human aglycosylated Fc, receptors in Escherichia coli,BIOTECHNOLOGY & BIOENGINEERING, Issue 1 2010Sang Taek Jung Abstract Effector Fc gamma receptors (Fc,Rs) are expressed on the surface of a variety of cells of hematopoietic lineage and serve as a bridge between adaptive and innate immune responses. The interaction between immune complexes, formed by IgG class antibodies that are crosslinked with antigen, and Fc,Rs triggers signaling cascades that result in numerous cellular responses including the activation or donwregulation of cytotoxic responses, cytokine release, and antibody synthesis. Here, the extracellular domains of the human type I transmembrane Fc,Rs were expressed in Escherichia coli and their interactions to subclass IgGs (IgG1, IgG2, IgG3, and IgG4) antibodies were analyzed. Expression using fully synthetic E. coli codon optimized Fc,R genes and optimization of sequences for N-terminal translation initiation region through mRNA secondary structure prediction enabled us to achieve high yield of purified, bacterially expressed receptors, including Fc,RI and Fc,RIIIa which have not been successfully expressed in bacteria until now. The aglycosylated Fc,Rs showed similar IgG subclass binding selectivity compared to the respective glycosylated Fc,Rs expressed in mammalian cells. Biotechnol. Bioeng. 2010;107: 21,30. © 2010 Wiley Periodicals, Inc. [source] Extracellular ATP and adenosine induce cell apoptosis of human hepatoma Li-7A cells via the A3 adenosine receptorBRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2003Long T Wen Extracellular ATP is a potent signaling molecule that modulates a myriad of cellular functions through the activation of P2 purinergic receptors and is cytotoxic to a variety of cells at higher concentrations. The mechanism of ATP-elicited cytotoxicity is not fully understood. In this study, we investigated the effect of extracellular ATP on the human hepatoma Li-7A cells. We observed a time- and dose-dependent growth inhibition of Li-7A cells by ATP, which is accompanied by an increase in the active form of caspase-3 as well as increased cleavage of its substrate, poly (ADP-ribose) polymerase. The cytotoxic effect of extracellular ATP was not mediated by the P2X7 receptor, since (1) the effect was not abolished by the P2X7 receptor antagonists oxidized ATP and KN-62, and (2) extracellular ADP, AMP, and adenosine were also cytotoxic. We found that ATP and ADP were degraded to adenosine by Li-7A cells and that treatment of Li-7A cells by adenosine resulted in growth inhibition and caspase-3 activation, indicating that adenosine is the apoptotic agent. Using adenosine receptor agonists and antagonists, as well as inhibitors of adenosine transport and deamination, we showed that the cytotoxic effect of adenosine is specifically mediated by the A3 receptor even though transcripts of A1, A2A, A2B, and a splice variant of the P2X7 receptors were detected in Li-7A cells by RT,PCR. Cytotoxicity caused by exogenous ATP and adenosine was completely abolished by the caspase-3 inhibitor Z-DEVD-FMK, demonstrating the central role of caspase-3 in apoptosis of Li-7A cells. British Journal of Pharmacology (2003) 140, 1009,1018. doi:10.1038/sj.bjp.0705523 [source] Functional analysis of mutants of the optineurin gene, associated with some forms of glaucomaACTA OPHTHALMOLOGICA, Issue 2008D BALASUBRAMANIAN Purpose Mutations in the gene OPTN are associated with normal tension and open angle glaucomas. We have studied the effects of some of these mutations on the cellular biology of retinal ganglion cells, and tried to infer the role of the protein optineurin. Methods We transfected plasmids expressing normal or wild-type (WT) and E50K, R545Q, H26D, and H486R mutant optineurin into a variety of cells such as HeLa, COS-1, retinal pigment epithelial (RPE), and the rat retinal ganglion cell (RGC) line RGC-5, and followed their effects on cell survival by morphologic observation of cells. Expression of optineurin and its mutants was monitored by immunofluorescence staining of cells and by Western blotting. Results The E50K mutant of optineurin, which is associated with the severest phenotype, was seen to selectively induce the death of retinal ganglion cells but not of the other cell lines tested. Neither the wild type cDNA nor the other mutants have any such effect. This cell death induced by E50K OPTN was inhibited by the antioxidants N-acetylcysteine and Trolox. E50K was seen to generate reactive oxygen species (ROS), which were reduced by antioxidants. Coexpression of manganese superoxide dismutase with the E50K mutant abolished ROS production and inhibited cell death. Conclusion E50K optineurin is a gain of function mutant, which has acquired the ability to induce cell death selectively in retinal ganglion cells. This cell death was mediated by oxidative stress. The present findings suggest the possibility of antioxidant use for delaying or controlling some forms of glaucoma. [source] Cysteinyl leukotrienes: multi-functional mediators in allergic rhinitisCLINICAL & EXPERIMENTAL ALLERGY, Issue 6 2006M. Peters-Golden Summary Cysteinyl leukotrienes (CysLTs) are a family of inflammatory lipid mediators synthesized from arachidonic acid by a variety of cells, including mast cells, eosinophils, basophils, and macrophages. This article reviews the data for the role of CysLTs as multi-functional mediators in allergic rhinitis (AR). We review the evidence that: (1) CysLTs are released from inflammatory cells that participate in AR, (2) receptors for CysLTs are located in nasal tissue, (3) CysLTs are increased in patients with AR and are released following allergen exposure, (4) administration of CysLTs reproduces the symptoms of AR, (5) CysLTs play roles in the maturation, as well as tissue recruitment, of inflammatory cells, and (6) a complex inter-regulation between CysLTs and a variety of other inflammatory mediators exists. [source] Eosinophil activation and cysteinyl leukotriene production in infants with respiratory syncytial virus bronchiolitisCLINICAL & EXPERIMENTAL ALLERGY, Issue 4 2004D. Dimova-Yaneva Summary Background It has been suggested that acute infantile bronchiolitis associated with respiratory syncytial virus (RSV) may share some pathogenic features with atopic asthma in that virus-specific IgE is produced and cysteinyl leukotrienes (cLTs) and eosinophil cationic protein (ECP) have been detected in airway secretions. ECP is a specific marker of eosinophil activation although leukotrienes can be released from a variety of cells including mast cells, eosinophils and monocytes. Objective To test the association between eosinophil activation and cysteinyl leukotriene production in the upper airway secretions of infants with RSV positive (RSV+ve) bronchiolitis. Methods Nasal lavage samples were performed in 78 infants (0.0,11.5 months) admitted to hospital with RSV+ve bronchiolitis soon after admission (0,48 h). Leukotriene C4 (LTC4) was assayed by enzyme immunoassay (EIA) and eosinophil cationic protein (ECP) by fluoroimmunoassay (FIA). Results LTC4 was detectable in 51 and ECP in 57 of 78 samples with a significant positive relationship between LTC4 and ECP (r=0.557, P<0.001). Conclusion In the majority of our subjects with RSV+ve bronchiolitis ECP and LTC4 were detectable in upper airway secretions and were significantly associated with each other. In this clinical setting much of the detected LTC4 within upper airway secretions is likely to originate from the eosinophil, an observation that may have implications for clinical management and for delineation of the underlying mechanisms associated with this illness. [source] | |||||||||||||