47 results found
Kay AB, Clark P, Maurer M, et al., 2015, Elevations in T-helper-2-initiating cytokines (interleukin-33, interleukin-25 and thymic stromal lymphopoietin) in lesional skin from chronic spontaneous ('idiopathic') urticaria, BRITISH JOURNAL OF DERMATOLOGY, Vol: 172, Pages: 1294-1302, ISSN: 0007-0963
Kay AB, Ying S, Ardelean E, et al., 2014, Elevations in vascular markers and eosinophils in chronic spontaneous urticarial weals with low-level persistence in uninvolved skin, BRITISH JOURNAL OF DERMATOLOGY, Vol: 171, Pages: 505-511, ISSN: 0007-0963
Kay AB, Ying S, Ardelean E, et al., 2014, Calcitonin gene-related peptide and vascular endothelial growth factor are expressed in lesional but not uninvolved skin in chronic spontaneous urticaria, CLINICAL AND EXPERIMENTAL ALLERGY, Vol: 44, Pages: 1053-1060, ISSN: 0954-7894
Clark P, 2014, Protease-mediated ectodomain shedding, THORAX, Vol: 69, Pages: 682-684, ISSN: 0040-6376
Bonner K, Pease JE, Corrigan CJ, et al., 2013, CCL17/thymus and activation-regulated chemokine induces calcitonin gene-related peptide in human airway epithelial cells through CCR4, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 132, Pages: 942-+, ISSN: 0091-6749
Elbediwy A, Zihni C, Terry SJ, et al., 2012, Epithelial junction formation requires confinement of Cdc42 activity by a novel SH3BP1 complex, J Cell Biol, Vol: 198, Pages: 677-693, ISSN: 1540-8140
Epithelial cell-cell adhesion and morphogenesis require dynamic control of actin-driven membrane remodeling. The Rho guanosine triphosphatase (GTPase) Cdc42 regulates sequential molecular processes during cell-cell junction formation; hence, mechanisms must exist that inactivate Cdc42 in a temporally and spatially controlled manner. In this paper, we identify SH3BP1, a GTPase-activating protein for Cdc42 and Rac, as a regulator of junction assembly and epithelial morphogenesis using a functional small interfering ribonucleic acid screen. Depletion of SH3BP1 resulted in loss of spatial control of Cdc42 activity, stalled membrane remodeling, and enhanced growth of filopodia. SH3BP1 formed a complex with JACOP/paracingulin, a junctional adaptor, and CD2AP, a scaffolding protein; both were required for normal Cdc42 signaling and junction formation. The filamentous actin-capping protein CapZ also associated with the SH3BP1 complex and was required for control of actin remodeling. Epithelial junction formation and morphogenesis thus require a dual activity complex, containing SH3BP1 and CapZ, that is recruited to sites of active membrane remodeling to guide Cdc42 signaling and cytoskeletal dynamics.
Bonner K, Kariyawasam HH, Ali FR, et al., 2010, Expression of functional receptor activity modifying protein 1 by airway epithelial cells with dysregulation in asthma, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 126, Pages: 1277-U314, ISSN: 0091-6749
Khamri W, Walker MM, Clark P, et al., 2010, Helicobacter pylori stimulates dendritic cells to induce interleukin-17 expression from CD4+ T lymphocytes., Infect Immun, Vol: 78, Pages: 845-853
Helicobacter pylori is a human gastroduodenal pathogen that leads to active chronic inflammation characterized by T-cell responses biased toward a Th1 phenotype. It has been accepted that H. pylori infection induces a Th17 response. At mucosal sites, dendritic cells (DCs) have the capacity to induce effector T cells. Here, we evaluate the role of DCs in the H. pylori-induced interleukin-17 (IL-17) response. Immunohistochemistry and immunofluorescence were performed on human gastric mucosal biopsy samples and showed that myeloid DCs in H. pylori-infected patients colocalized with IL-23- and that IL-17-producing lymphocytes were present in H. pylori-infected antral biopsy samples. In parallel, human monocyte-derived DCs stimulated in vitro with live H. pylori cells produced significant levels of IL-23 in the absence of IL-12 release. The subsequent incubation of H. pylori-infected DCs with autologous CD4(+) T cells led to gamma interferon (IFN-gamma) and IL-17 expression. The inhibition of IL-1 and, to a lesser extent, IL-23 inhibited IL-17 production by T cells. Finally, isogenic H. pylori mutant strains not expressing major virulence factors were less effective in inducing IL-1 and IL-23 release by DCs and IL-17 release by T cells than parental strains. Altogether, we can conclude that DCs are potent inducers of IL-23/IL-17 expression following H. pylori stimulation. IL-1/IL-23 as well as H. pylori virulence factors seem to play an important role in mediating this response.
Reynolds C, Barkans J, Clark P, et al., 2009, Natural killer T cells in bronchial biopsies from human allergen challenge model of allergic asthma., J Allergy Clin Immunol, Vol: 124, Pages: 860-862
Durrenberger PF, Filiou MD, Moran LB, et al., 2009, DnaJB6 Is Present in the Core of Lewy Bodies and Is Highly Up-Regulated in Parkinsonian Astrocytes, JOURNAL OF NEUROSCIENCE RESEARCH, Vol: 87, Pages: 238-245, ISSN: 0360-4012
Anderson PJB, Watts HR, Hille CJ, et al., 2008, Glial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat., Clinical Ophthalmology, Vol: 2, Pages: 801-816
The effects of an intravitreal or subretinal injection of soluble or aggregated forms of Aβ1–42 on retinal nestin-immunoreactivity (-IR) and glial fi brillary acidic protein (GFAP)-IR in astrocytes and Müller glial cells and the integrity of the blood-retinal barrier (BRB) were tested in the in vivo rat vitreal-retinal model. Retinas were exposed for 1, 2, 3, 5 or 30 days. We present novel data demonstrating that aggregated Aβ1–42 up-regulates nestin-IR in astrocytes and Müller cells, with a graded response directly related to the length of pre-injection aggregation time. Similar results were obtained with GFAP-IR, but the signal was weaker. An intravitreal injection of aggregated Aβ1–42 led to VEGF-IR up-regulation, particularly in the GCL and to a lesser extent in the INL. VEGFR1-IR (Flt1) was also increased, particularly in Müller cells and this was accompanied by marked leakage of albumin into the retinal parenchyma of the injected eye, but not in the contralateral eye.
Meiser A, Mueller A, Wise EL, et al., 2008, The chemokine receptor CXCR3 is degraded following internalization and is replenished at the cell surface by de novo synthesis of receptor, JOURNAL OF IMMUNOLOGY, Vol: 180, Pages: 6713-6724, ISSN: 0022-1767
Glyn MC, Lawrenson JG, Ward BJ, et al., 2008, Rho kinase-mediated reduction in cardiac capillary endothelial cell dimensions, in situ, against flow, MICROCIRCULATION, Vol: 15, Pages: 175-190, ISSN: 1073-9688
Walker M, Ellis S, Auza MJ, et al., 2008, The intercellular adhesion molecule, Cadherin-10, is a marker for human prostate luminal epithelial cells that is not expressed in prostate cancer., Modern Pathology
Millan J, Hewlett L, Glyn M, et al., 2006, Lymphocyte transcellular migration occurs through recruitment of endothelial ICAM-1 to caveola- and F-actin-rich domains, NATURE CELL BIOLOGY, Vol: 8, Pages: 113-U5, ISSN: 1465-7392
Williams MJ, Lowrie MB, Bennett JP, et al., 2005, Cadherin-10 is a novel blood-brain barrier adhesion molecule in human and mouse, BRAIN RESEARCH, Vol: 1058, Pages: 62-72, ISSN: 0006-8993
Weller CL, Collington SJ, Brown JK, et al., 2005, Leukotriene B-4, an activation product of mast cells, is a chemoattractant for their progenitors, Journal of Experimental Medicine, Vol: 201, Pages: 1961-1971, ISSN: 1540-9538
Mast cells are tissue-resident cells with important functions in allergy and inflammation. Pluripotential hematopoietic stem cells in the bone marrow give rise to committed mast cell progenitors that transit via the blood to tissues throughout the body, where they mature. Knowledge is limited about the factors that release mast cell progenitors from the bone marrow or recruit them to remote tissues. Mouse femoral bone marrow cells were cultured with IL-3 for 2 wk and a range of chemotactic agents were tested on the c-kit+ population. Cells were remarkably refractory and no chemotaxis was induced by any chemokines tested. However, supernatants from activated mature mast cells induced pronounced chemotaxis, with the active principle identified as leukotriene (LT) B4. Other activation products were inactive. LTB4 was highly chemotactic for 2-wk-old cells, but not mature cells, correlating with a loss of mRNA for the LTB4 receptor, BLT1. Immature cells also accumulated in vivo in response to intradermally injected LTB4. Furthermore, LTB4 was highly potent in attracting mast cell progenitors from freshly isolated bone marrow cell suspensions. Finally, LTB4 was a potent chemoattractant for human cord blood–derived immature, but not mature, mast cells. These results suggest an autocrine role for LTB4 in regulating tissue mast cell numbers.
Dye JF, Lawrence L, Linge C, et al., 2004, Distinct patterns of microvascular endothelial cell morphology are determined by extracellular matrix composition, ENDOTHELIUM-JOURNAL OF ENDOTHELIAL CELL RESEARCH, Vol: 11, Pages: 151-167, ISSN: 1062-3329
Andersson KG, Roed J, Byrne MA, et al., 2004, Airborne Contamination in the indoor environment and its implications for dose, Riso-R Report
Dye JF, Vause S, Johnston T, et al., 2004, Characterization of cationic amino acid transporters and expression of endothelial nitric oxide synthase in human placental microvascular endothelial cells, FASEB JOURNAL, Vol: 18, Pages: 125-127, ISSN: 0892-6638
Clark P, 2004, Cell Motility:from molecules to organisms, Chichester, England, UK, Publisher: John Wiley and Sons, ISBN: 9780470848722
Williams MJ, Clark P, 2003, Microscopic analysis of the cellular events during scatter factor/hepatocyte growth factor-induced epithelial tubulogenesis, JOURNAL OF ANATOMY, Vol: 203, Pages: 483-503, ISSN: 0021-8782
Dye JF, Vause S, Johnston T, et al., 2003, Characterization of cationic amino acid transporters and expression of endothelial nitric oxide synthase in human placental microvascular endothelial cells, FASEB JOURNAL, Vol: 17, Pages: 125-+, ISSN: 0892-6638
Clark P, Dunn GA, Knibbs A, et al., 2002, Alignment of myoblasts on ultrafine gratings inhibits fusion in vitro, INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, Vol: 34, Pages: 816-825, ISSN: 1357-2725
Pook MA, Al-Mahdawi S, Carroll CJ, et al., 2001, Rescue of the Friedreich's ataxia knockout mouse by human YAC transgenesis, NEUROGENETICS, Vol: 3, Pages: 185-193, ISSN: 1364-6745
Dye JF, Leach L, Clark P, et al., 2001, Cyclic AMP and acidic fibroblast growth factor have opposing effects on tight and adherens junctions in microvascular endothelial cells in vitro, MICROVASCULAR RESEARCH, Vol: 62, Pages: 94-113, ISSN: 0026-2862
Dye JF, Jablenska R, Donnelly JL, et al., 2001, Phenotype of the endothelium in the human term placenta, PLACENTA, Vol: 22, Pages: 32-43, ISSN: 0143-4004
Clark P, Coles D, Peckham M, 1997, Preferential adhesion to and survival on patterned laminin organizes myogenesis in vitro, EXPERIMENTAL CELL RESEARCH, Vol: 230, Pages: 275-283, ISSN: 0014-4827
GALUSTIAN C, DYE J, LEACH L, et al., 1995, ACTIN CYTOSKELETAL ISOFORMS IN HUMAN ENDOTHELIAL-CELLS IN-VITRO - ALTERATION WITH CELL PASSAGE, IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL, Vol: 31, Pages: 796-802, ISSN: 1071-2690
WEBB A, CLARK P, SKEPPER J, et al., 1995, GUIDANCE OF OLIGODENDROCYTES AND THEIR PROGENITORS BY SUBSTRATUM TOPOGRAPHY, JOURNAL OF CELL SCIENCE, Vol: 108, Pages: 2747-2760, ISSN: 0021-9533
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