Research Topics
Genomes and Genes | Janette K BurgessSummaryAffiliation: University of Sydney Country: Australia Publications
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Publications
Connective tissue growth factor induces extracellular matrix in asthmatic airway smooth musclePeter R A Johnson
Department of Pharmacology, The University of Sydney, NSW, Australia
Am J Respir Crit Care Med 173:32-41. 2006..Our results suggest that these two cytokines may be important in the deposition of extracellular matrix proteins and that the signal transduction pathways may be different in asthmatic and nonasthmatic cells...- Extracellular matrix regulates enhanced eotaxin expression in asthmatic airway smooth muscle cellsVivien Chan
King's College London School of Medicine, MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, Thomas Guy House, Guy's Hospital Campus, London SE1 9RT, UK
Am J Respir Crit Care Med 174:379-85. 2006..CONCLUSION: The data indicate that ASM cells cultured from subjects with asthma are hypersecretory compared with cells from healthy donors and that autocrine fibronectin secretion acting via alpha5beta1 in part underlies this effect... - New developments in the analysis of gene expressionJ K Burgess
Department of Pharmacology, University of Sydney, New South Wales, Australia
Redox Rep 5:63-73. 2000..Molecules found to be associated with defined pathological lesions may provide clues about new therapeutic targets in the future... - Connective tissue growth factor and vascular endothelial growth factor from airway smooth muscle interact with the extracellular matrixJanette K Burgess
Respiratory Research Group, Department of Pharmacology, University of Sydney, Sydney, NSW, Australia 2006
Am J Physiol Lung Cell Mol Physiol 290:L153-61. 2006..This relationship has the potential to contribute to the changes that constitute airway remodeling, therefore providing a novel focus for therapeutic intervention in asthma... - Connective tissue growth factor: a role in airway remodelling in asthma?Janette K Burgess
Department of Pharmacology, University of Sydney and Woolcock Institute of Medical Research, Sydney, New South Wales, Australia
Clin Exp Pharmacol Physiol 32:988-94. 2005..5. Current asthma therapies do not inhibit CTGF induction. 6. Understanding the mechanisms underlying the role of CTGF in airway remodelling may lead to new therapeutic strategies for asthma... 
Reduction of tumstatin in asthmatic airways contributes to angiogenesis, inflammation, and hyperresponsivenessJanette K Burgess
Respiratory Research Group, Discipline of Pharmacology, Bosch Building, D05, University of Sydney, Sydney, NSW, Australia 2006
Am J Respir Crit Care Med 181:106-15. 2010..Collagen IV is decreased in the airway basement membrane in asthma. It has six alpha chains, of which the noncollagenous domain-1 domains have endogenous antiangiogenic properties...- A phosphodiesterase 4 inhibitor inhibits matrix protein deposition in airways in vitroJanette K Burgess
Department of Pharmacology, University of Sydney, NSW, Australia
J Allergy Clin Immunol 118:649-57. 2006..Airway smooth muscle (ASM) cells may contribute to airway remodeling through the release of growth factors, cytokines, and extracellular matrix (ECM) proteins. The effect of current asthma therapies on this release is not known... - Tissue and matrix influences on airway smooth muscle functionJanette K Burgess
Discipline of Pharmacology, Bosch Institute, University of Sydney, Sydney, Australia
Pulm Pharmacol Ther 22:379-87. 2009..This review summarises our current understanding of the influence of the ECM on ASM function... - The role of the extracellular matrix and specific growth factors in the regulation of inflammation and remodelling in asthmaJanette K Burgess
Discipline of Pharmacology, The University of Sydney, Woolcock Institute of Medical Research and the Cooperative Research Centre for Asthma and Airways, Sydney, NSW Australia
Pharmacol Ther 122:19-29. 2009..This review aims to summarise the role growth factors and extracellular matrix proteins play in the regulation of inflammation and airway remodelling in the asthmatic airway... - Expression of connective tissue growth factor in asthmatic airway smooth muscle cellsJanette K Burgess
Department of Pharmacology, University of Sydney, Sydney, Australia
Am J Respir Crit Care Med 167:71-7. 2003.... - Molecular mechanisms of drug-induced thrombocytopeniaJ K Burgess
Department of Pharmacology, University of Sydney, Sydney, New South Wales, Australia
Curr Opin Hematol 8:294-8. 2001..Identification of antibody binding sites will enhance our understanding of the pathogenesis of immune drug-induced thrombocytopenia... - Gene expression studies using microarraysJ K Burgess
Respiratory Research Group, Department of Pharmacology, University of Sydney, New South Wales, Australia
Clin Exp Pharmacol Physiol 28:321-8. 2001..This increase in knowledge about gene function will allow new targeted approaches for the development of drugs and/or gene therapies... - CD40 and OX40 ligand are increased on stimulated asthmatic airway smooth muscleJanette K Burgess
Department of Pharmacology, University of Sydney, Sydney, NSW, Australia
J Allergy Clin Immunol 115:302-8. 2005..These cytokines have the potential to alter the expression of surface receptors such as CD40 and OX40 ligand on the airway smooth muscle cell... - TGFβ1 induces IL-6 and inhibits IL-8 release in human bronchial epithelial cells: the role of Smad2/3Qi Ge
Respiratory Research Group, Discipline of Pharmacology, Faculty of Medicine, The University of Sydney, Sydney, NSW, Australia
J Cell Physiol 225:846-54. 2010..Understanding the mechanism of aberrant pro-inflammatory cytokine production in asthmatic airways will allow the development of alternative ways to control airway inflammation... - The phosphoinositide 3'-kinase p110δ modulates contractile protein production and IL-6 release in human airway smooth muscleQi Ge
Woolcock Institute of Medical Research, The University of Sydney, Sydney, NSW, Australia
J Cell Physiol 227:3044-52. 2012.... - Rhinovirus infection induces extracellular matrix protein deposition in asthmatic and nonasthmatic airway smooth muscle cellsCurtis Kuo
Discipline of Pharmacology, University of Sydney, Camperdown, Australia
Am J Physiol Lung Cell Mol Physiol 300:L951-7. 2011..Our results suggest that viruses may contribute to airway remodeling through increased ECM deposition, which in turn may contribute to increased ASM mass via increased cell migration... - β2-Agonists upregulate PDE4 mRNA but not protein or activity in human airway smooth muscle cells from asthmatic and nonasthmatic volunteersKyoko Niimi
Cell Biology Group, Woolcock Institute of Medical Research, School of Medical Sciences, The Univ of Sydney, Sydney, NSW, Australia
Am J Physiol Lung Cell Mol Physiol 302:L334-42. 2012..This leads us to speculate that continual therapy with β2AR agonists is unlikely to cause PDE4-mediated tachyphylaxis... - TGF-β enhances deposition of perlecan from COPD airway smooth muscleYukikazu Ichimaru
Cell Biology Group, Woolcock Institute of Medical Research, NSW, Australia
Am J Physiol Lung Cell Mol Physiol 302:L325-33. 2012..Seeding on perlecan domains did not increase proliferation of any ASMC type. TGF-β(1)-induced perlecan deposition may enhance attachment of migrating ASMC in vivo and thus may be a mechanism for ASMC layer hypertrophy in COPD... - Dysfunctional interaction of C/EBPalpha and the glucocorticoid receptor in asthmatic bronchial smooth-muscle cellsMichael Roth
Department of Pharmacology and the Woolcock Institute of Medical Research, University of Sydney, Sydney, Australia
N Engl J Med 351:560-74. 2004..We examined the signaling pathway controlling the inhibitory effect of glucocorticoids on cell proliferation and interleukin-6 synthesis in bronchial smooth-muscle cells of subjects with asthma and those without asthma... - Phosphatidylinositol 3-kinase isoform-specific effects in airway mesenchymal cell functionLyn M Moir
Woolcock Institute of Medical Research, Sydney, Australia
J Pharmacol Exp Ther 337:557-66. 2011..In addition, PIK75 decreased cell survival in TGFβ-stimulated asthmatic, but not nonasthmatic, ASM cells. In conclusion, specific PI3K isoforms may play a role in pathophysiological events relevant to airway wall remodeling... - Extracellular matrix proteins modulate asthmatic airway smooth muscle cell proliferation via an autocrine mechanismPeter R A Johnson
Department of Pharmacology, University of Sydney, Sydney, NSW 2006, Australia
J Allergy Clin Immunol 113:690-6. 2004..These changes are likely to contribute to the airway wall remodeling that occurs in asthma... 
Asthmatic airway smooth muscle CXCL10 production: mitogen-activated protein kinase JNK involvementYazan A Alrashdan
Respiratory Research Group, Faculty of Pharmacy, University of Sydney, Sydney, NSW 2006, Australia
Am J Physiol Lung Cell Mol Physiol 302:L1118-27. 2012..However, in both, JNK activation did not regulate early events leading to NF-κB activation. Thus JNK and NF-κB provide independent therapeutic targets for limiting CXCL10 production and mast cell migration to the ASM in asthma...- Rhinovirus-induced exacerbations of asthma: How is the {beta}2-adrenoceptor implicated?Thomas Trian
The University of Sydney, NSW, Australia
Am J Respir Cell Mol Biol 43:227-33. 2010.... 
Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infectionBrian G G Oliver
Department of Pharmacology, University of Sydney, NSW, 2006, Australia
Respir Res 7:71. 2006..We hypothesised that rhinovirus induction of inflammatory cytokine release from airway smooth muscle is augmented and differentially regulated in asthmatic compared to normal HASM cells...- Dual ERK and phosphatidylinositol 3-kinase pathways control airway smooth muscle proliferation: differences in asthmaJanette K Burgess
Respiratory Research Group, Discipline of Pharmacology, Faculty of Medicine, University of Sydney, Sydney, NSW, Australia
J Cell Physiol 216:673-9. 2008..This study suggests that the PI 3-kinase pathway may be an attractive target for reversing hyperplasia in asthma... - Is low dose inhaled corticosteroid therapy as effective for inflammation and remodeling in asthma? A randomized, parallel group studyMelissa Baraket
Woolcock Institute of Medical Research, Sydney, NSW, Australia
Respir Res 13:11. 2012..Although symptom/lung function response to low and high dose ICS medication is comparable, it is uncertain whether low dose ICSs are as effective as high dose in the treatment of inflammation and remodeling... - Fibulin-1 is increased in asthma--a novel mediator of airway remodeling?Justine Y Lau
Cooperative Research Centre for Asthma and Airways, Sydney, New South Wales, Australia
PLoS ONE 5:e13360. 2010..There are four isoforms in humans (A-D) of which fibulin-1C and 1D predominate. The objective of this study was to study the expression of fibulin-1 in volunteers with and without asthma, and to examine its function in vitro... - The effect of asthma therapeutics on signalling and transcriptional regulation of airway smooth muscle functionAlaina J Ammit
Respiratory Research Group, Faculty of Pharmacy, University of Sydney, NSW, Australia
Pulm Pharmacol Ther 22:446-54. 2009..This review is an overview of the effects of current therapies, and some of those in development, on key signalling pathways and transcription factors involved in these ASM functions... - Effect of IL-6 trans-signaling on the pro-remodeling phenotype of airway smooth muscleAlaina J Ammit
Faculty of Pharmacy, University of Sydney, Sydney, NSW 2006, Australia
Am J Physiol Lung Cell Mol Physiol 292:L199-206. 2007..As levels of sIL-6Ralpha are increased in asthma, this demonstration of IL-6 trans-signaling in ASM has relevance to the development of airway remodeling... - Detection and characterization of OX40 ligand expression in human airway smooth muscle cells: a possible role in asthma?Janette K Burgess
Respiratory Research Group, Department of Pharmacology, Bosch Building D05, University of Sydney, Sydney, NSW 2006, Australia
J Allergy Clin Immunol 113:683-9. 2004..Cell-surface molecules play an important role in the development of an immune response. A number of cell-surface molecules are expressed on ASM cells, and these might contribute to the inflammatory reaction... - β2-Agonist induced cAMP is decreased in asthmatic airway smooth muscle due to increased PDE4DThomas Trian
Cell Biology, Woolcock Institute of Medical Research, Sydney, New South Wales, Australia
PLoS ONE 6:e20000. 2011..In addition, some studies have suggested impaired β-agonist induced ASM relaxation in asthmatics, but the mechanism is not known... - Rhinovirus infection induces expression of airway remodelling factors in vitro and in vivoCurtis Kuo
Discipline of Pharmacology, The University of Sydney, Camperdown, UK
Respirology 16:367-77. 2011..Viral infections may promote the development of asthma and are the most common causes of asthma exacerbations. We evaluated whether rhinovirus (RV) infection induces airway remodelling, as assessed by ECM deposition... - Increased sensitivity of asthmatic airway smooth muscle cells to prostaglandin E2 might be mediated by increased numbers of E-prostanoid receptorsJanette K Burgess
Respiratory Research Group, Department of Pharmacology, Bosch Building D05, University of Sydney, Sydney, NSW 2006, Australia
J Allergy Clin Immunol 113:876-81. 2004..In contrast, these cells have increased sensitivity. This increased sensitivity might be mediated by the increased numbers of EP2 receptors on the surface... - Comparison of gel contraction mediated by airway smooth muscle cells from patients with and without asthmaHisako Matsumoto
Discipline of Pharmacology, University of Sydney, NSW 2006, Australia
Thorax 62:848-54. 2007..The purpose of this study was to establish a method to measure contraction of ASM cells by embedding them into a collagen gel, and to compare the contraction between subjects with and without asthma... - Matrix proteins from smoke-exposed fibroblasts are pro-proliferativeDavid I Krimmer
Woolcock Institute of Medical Research Cell Biology, Sydney, New South Wales, Australia
Am J Respir Cell Mol Biol 46:34-9. 2012..ECM produced from COPD fibroblasts after CSE exposure has proproliferative effects. Thus, the ECM in patients with COPD may create an environment that promotes airway remodeling... - Differential expression of peroxisome proliferator activated receptor gamma and cyclin D1 does not affect proliferation of asthma- and non-asthma-derived airway smooth muscle cellsJustine Y Lau
Cooperative Research Centre for Asthma and Airways, The University of Sydney, Sydney, New South Wales, Australia
Respirology 15:303-12. 2010..In the presence of FBS, PPARgamma levels were higher in subconfluent asthma-derived cells but lower in confluent cells compared with non-asthma-derived. However, PPARgamma activation did not alter cell proliferation... - Transforming growth factor beta 1 increases fibronectin deposition through integrin receptor alpha 5 beta 1 on human airway smooth muscleLyn M Moir
Woolcock Institute of Medical Research, University of Sydney, Sydney, Australia
J Allergy Clin Immunol 121:1034-9.e4. 2008..Altered expression of the integrin receptors, such as the fibronectin receptor alpha(5)beta(1), might be implicated in extracellular matrix accumulation in airway remodeling in asthma... - Airway smooth muscle and fibroblasts in the pathogenesis of asthmaPeter R A Johnson
Department of Pharmacology, The University of Sydney, NSW Australia 2006
Curr Allergy Asthma Rep 4:102-8. 2004..Current asthma therapies lack the ability to completely prevent or reverse the remodeling of the airways, therefore indicating the need for new therapeutic strategies to counter this important aspect of asthma... - Interaction between glucocorticoids and beta2 agonists on bronchial airway smooth muscle cells through synchronised cellular signallingMichael Roth
Department of Pharmacology and the Woolcock Institute of Medical Research, University of Sydney, NSW 2006, Australia
Lancet 360:1293-9. 2002..Our aim was to elucidate how glucocorticoids and beta2 agonists affect the growth of human bronchial airway smooth muscle cells... - Airway smooth muscle--its relationship to the extracellular matrixJudith L Black
Department of Pharmacology, Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW 2006, Australia
Respir Physiol Neurobiol 137:339-46. 2003..It is unlikely that current therapy is effective in preventing or reversing remodeling, and therefore, understanding the pathophysiological events, which underlie its mechanism is critical... - Elastin in asthmaCaroline J Reddel
School of Molecular Bioscience, University of Sydney, Sydney, NSW 2006, Australia
Pulm Pharmacol Ther 25:144-53. 2012..This review summarises the current understanding of the role of elastin in the asthmatic airway... - Cyclosporine A mediates fibroproliferation through epithelial cellsKatrin E Hostettler
Respiratory Research Group, Department of Pharmacology, University of Sydney, New South Wales 2006, Australia
Transplantation 77:1886-93. 2004..Epithelium-fibroblast interactions have been suggested to play a crucial role in the course of fibroproliferation, which is a major feature of OB... - ERK1/2 and p38 MAP kinase control MMP-2, MT1-MMP, and TIMP action and affect cell migration: a comparison between mesothelioma and mesothelial cellsJun Zhong
Department of Pharmacology, The Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia
J Cell Physiol 207:540-52. 2006..Mesothelioma progression depends on an interaction with mesothelial cells that provide MT1-MMP necessary to activate pro-MMP-2 to facilitate migration through an extracellular matrix (ECM) layer... - Thiazolidinediones inhibit airway smooth muscle release of the chemokine CXCL10: in vitro comparison with current asthma therapiesPetra Seidel
Respiratory Research Group, Faculty of Pharmacy, The University of Sydney, A15, Science Rd, Sydney, NSW 2006, Australia
Respir Res 13:90. 2012..abstract:.. - Combined Beta-agonists and corticosteroids do not inhibit extracellular matrix protein production in vitroQi Ge
Division of Cell Biology, Woolcock Institute of Medical Research, Sydney, P O Box M77, Missenden Road, NSW 2050, Australia
J Allergy (Cairo) 2012:403059. 2012..TGFβ1-induced IL-6 release was inhibited by the combination of drugs. Conclusion. Current combination asthma therapies are unable to prevent or reverse remodeling events regulated by ASM cells... - Analysis of gene expressionJanette K Burgess
Respiratory Research Group, Department of Pharmacology, University of Sydney, Sydney, New South Wales, 2006 Australia
Methods Enzymol 356:259-70. 2002 - Effects of β(2) Agonists, Corticosteroids, and Novel Therapies on Rhinovirus-Induced Cytokine Release and Rhinovirus Replication in Primary Airway FibroblastsDavid Van Ly
Respiratory Research Group, Discipline of Pharmacology, The University of Sydney, Sydney, NSW 2006, Australia
J Allergy (Cairo) 2011:457169. 2011..Dimethylfumarate increased RV replication whilst other drugs did not alter RV replication. These data suggest that inhibition of NF-κB alone is unlikely to be an effective treatment compared to current asthma therapeutics... - Matrikines and the lungsJanette K Burgess
Cell Biology, Woolcock Institute of Medical Research, Sydney, NSW, Australia
Pharmacol Ther 134:317-37. 2012..The focus of this review will be to summarise our current understanding of the role, and potential for highly relevant actions, of matrikines in lung health and disease... - Disease-specific expression and regulation of CCAAT/enhancer-binding proteins in asthma and chronic obstructive pulmonary diseasePeter Borger
Pulmonary Cell Research, Department of Research and Pneumology, Department of Internal Medicine, University Hospital Basel, Basel, Switzerland
J Allergy Clin Immunol 119:98-105. 2007..CCAAT/enhancer-binding proteins (C/EBPs) control cell proliferation; lack of C/EBPalpha correlates with increased proliferation of bronchial smooth muscle cells (BSMCs) of asthmatic patients... - PAR-2 activation, PGE2, and COX-2 in human asthmatic and nonasthmatic airway smooth muscle cellsLinda S Chambers
Dept of Pharmacology, Univ of Sydney, New South Wales 2006, Australia
Am J Physiol Lung Cell Mol Physiol 285:L619-27. 2003..In addition, ASM cells from asthmatic patients produce significantly less PGE2 and COX-2 compared with nonasthmatic cells. These findings may contribute to the increase in muscle mass evident in asthmatic airways...