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Loss of ELK1 has differential effects on age-dependent organ fibrosis (2019)
Journal Article
Cairns, J. T., Habgood, A., Edwards-Pritchard, R. C., Joseph, C., John, A. E., Wilkinson, C., …Tatler, A. L. (2020). Loss of ELK1 has differential effects on age-dependent organ fibrosis. International Journal of Biochemistry and Cell Biology, 120, https://doi.org/10.1016/j.biocel.2019.105668

© 2019 The Author(s) ETS domain-containing protein-1 (ELK1) is a transcription factor important in regulating αvβ6 integrin expression. αvβ6 integrins activate the profibrotic cytokine Transforming Growth Factor β1 (TGFβ1) and are increased in the al... Read More about Loss of ELK1 has differential effects on age-dependent organ fibrosis.

The Its Not JUST Idiopathic pulmonary fibrosis Study (INJUSTIS): Description of the protocol for a multicentre prospective observational cohort study identifying biomarkers of progressive fibrotic lung disease (2019)
Journal Article
Khan, F., Stewart, I., Howard, L., McKeever, T., Jones, S., Hearson, G., …Saini, G. (2019). The Its Not JUST Idiopathic pulmonary fibrosis Study (INJUSTIS): Description of the protocol for a multicentre prospective observational cohort study identifying biomarkers of progressive fibrotic lung disease. BMJ Open Respiratory Research, 6(1), 1-7. doi:10.1136/bmjresp-2019-000439

Introduction: The Its Not JUST Idiopathic pulmonary fibrosis Study (INJUSTIS) is a multicentre, prospective, observational cohort study. The aims of this study are to identify genetic, serum and other biomarkers that may identify specific molecular m... Read More about The Its Not JUST Idiopathic pulmonary fibrosis Study (INJUSTIS): Description of the protocol for a multicentre prospective observational cohort study identifying biomarkers of progressive fibrotic lung disease.

Patient reported distress can aid clinical decision making in idiopathic pulmonary fibrosis: analysis of the PROFILE cohort (2019)
Journal Article
Stewart, I., McKeever, T., Braybrooke, R., Oballa, E., Simpson, J. K., Maher, T. M., …Saini, G. (2019). Patient reported distress can aid clinical decision making in idiopathic pulmonary fibrosis: analysis of the PROFILE cohort. European Respiratory Journal, 53(5), doi:10.1183/13993003.01925-2018

Idiopathic pulmonary fibrosis is a progressive and fatal interstitial lung disease. We aimed to determine if patient response to a palliative assessment survey could predict disease progression or death. We undertook a cross-sectional study in a U... Read More about Patient reported distress can aid clinical decision making in idiopathic pulmonary fibrosis: analysis of the PROFILE cohort.

Patient reported distress can aid clinical decision making in idiopathic pulmonary fibrosis: analysis of the PROFILE cohort (2018)
Other
Stewart, I., McKeever, T., Braybrooke, R., Oballa, E., Simpson, J. K., Maher, T. M., …Saini, G. (2018). Patient reported distress can aid clinical decision making in idiopathic pulmonary fibrosis: analysis of the PROFILE cohort

Idiopathic pulmonary fibrosis is a progressive and fatal interstitial lung disease. We aimed to determine if patient response to a palliative assessment survey could predict disease progression or death. We undertook a cross-sectional study in a U... Read More about Patient reported distress can aid clinical decision making in idiopathic pulmonary fibrosis: analysis of the PROFILE cohort.

Suberanilohydroxamic acid prevents TGF-β1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation (2018)
Journal Article
Pasini, A., Brand, O. J., Jenkins, G., Knox, A. J., & Pang, L. (2018). Suberanilohydroxamic acid prevents TGF-β1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation. BBA - Biochimica et Biophysica Acta, 1861(5), doi:10.1016/j.bbagrm.2018.03.007

Cyclooxygenase-2 (COX-2), with its main antifibrotic metabolite PGE, is regarded as an antifibrotic gene. Repressed COX-2 expression and deficient PGE have been shown to contribute to the activation of lung fibroblasts and excessive deposition of col... Read More about Suberanilohydroxamic acid prevents TGF-β1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation.

An epithelial biomarker signature for idiopathic pulmonary fibrosis: an analysis from the multicentre PROFILE cohort study (2017)
Journal Article
Maher, T. M., Oballa, E., Simpson, J. K., Porte, J., Habgood, A., Fahy, W. A., …Jenkins, R. G. (in press). An epithelial biomarker signature for idiopathic pulmonary fibrosis: an analysis from the multicentre PROFILE cohort study. Lancet Respiratory Medicine, 5(12), doi:10.1016/S2213-2600(17)30430-7

Background: Idiopathic Pulmonary Fibrosis (IPF) is a progressive, fatal condition with a variable disease trajectory. The aim of this study was to evaluate potential biomarkers that predict outcome for people with IPF. Method: The PROFILE study is a... Read More about An epithelial biomarker signature for idiopathic pulmonary fibrosis: an analysis from the multicentre PROFILE cohort study.

ECM crosslinking enhances fibroblast growth and protects against matrix proteolysis in lung fibrosis (2017)
Journal Article
Philp, C. J., Siebeke, I., Clements, D., Miller, S., Habgood, A., John, A. E., …Johnson, S. R. (2018). ECM crosslinking enhances fibroblast growth and protects against matrix proteolysis in lung fibrosis. American Journal of Respiratory Cell and Molecular Biology, 58(5), 594–603. doi:10.1165/rcmb.2016-0379OC

Idiopathic pulmonary fibrosis (IPF) is characterised by accumulation of extra cellular matrix (ECM) proteins and fibroblast proliferation. ECM cross-linking enzymes have been implicated in fibrotic diseases and we hypothesised that the ECM in IPF is... Read More about ECM crosslinking enhances fibroblast growth and protects against matrix proteolysis in lung fibrosis.

Genetic variants associated with susceptibility to idiopathic pulmonary fibrosis in people of European ancestry: a genome-wide association study (2017)
Journal Article
Allen, R. J., Porte, J., Braybrooke, R., Flores, C., Fingerlin, T. E., Oldham, J. M., …Jenkins, R. G. (2017). Genetic variants associated with susceptibility to idiopathic pulmonary fibrosis in people of European ancestry: a genome-wide association study. Lancet Respiratory Medicine, 5(11), doi:10.1016/S2213-2600(17)30387-9

Background Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease with high mortality, uncertain cause, and few treatment options. Studies have identified a significant genetic risk associated with the development of IPF; however,... Read More about Genetic variants associated with susceptibility to idiopathic pulmonary fibrosis in people of European ancestry: a genome-wide association study.

Interplay between EZH2 and G9a regulates CXCL10 gene repression in idiopathic pulmonary fibrosis (2017)
Journal Article
Coward, W. R., Brand, O. J., Pasini, A., Jenkins, G., Knox, A. J., & Pang, L. (in press). Interplay between EZH2 and G9a regulates CXCL10 gene repression in idiopathic pulmonary fibrosis. American Journal of Respiratory Cell and Molecular Biology, doi:10.1165/rcmb.2017-0286OC

Selective repression of the antifibrotic gene CXCL10 contributes to tissue remodelling in idiopathic pulmonary fibrosis (IPF). We have previously reported that histone deacetylation and histone H3 lysine 9 (H3K9) methylation are involved in CXCL10 re... Read More about Interplay between EZH2 and G9a regulates CXCL10 gene repression in idiopathic pulmonary fibrosis.

Effect of epigenetic inhibitors on lung fibroblast phenotype change in idiopathic pulmonary fibrosis (2016)
Journal Article
Pasini, A., Brand, O. J., Jenkins, G., Knox, A. J., & Pang, L. (2016). Effect of epigenetic inhibitors on lung fibroblast phenotype change in idiopathic pulmonary fibrosis. Thorax, 71(Supp3), doi:10.1136/thoraxjnl-2016-209333.59

Introduction and objectives: Idiopathic Pulmonary Fibrosis (IFP) is a fatal interstitial lung disease with unknown aetiology. Lung myofibroblasts (activated fibrobalsts) are the major effector cells in the pathogenesis of IPF. Transforming growth fac... Read More about Effect of epigenetic inhibitors on lung fibroblast phenotype change in idiopathic pulmonary fibrosis.

Effect of epigenetic inhibitors on lung fibroblast phenotype change in idiopathic pulmonary fibrosis (2016)
Journal Article
Pasini, A., Brand, O. J., Jenkins, G., Knox, A. J., & Pang, L. (2016). Effect of epigenetic inhibitors on lung fibroblast phenotype change in idiopathic pulmonary fibrosis. Thorax, 71(Suppl. 3), A32. doi:10.1136/thoraxjnl-2016-209333.59

Introduction and objectives: Idiopathic Pulmonary Fibrosis (IFP) is a fatal interstitial lung disease with unknown aetiology. Lung myofibroblasts (activated fibrobalsts) are the major effector cells in the pathogenesis of IPF. Transforming growth fac... Read More about Effect of epigenetic inhibitors on lung fibroblast phenotype change in idiopathic pulmonary fibrosis.

Suberanilohydroxamic acid (SAHA) inhibits collagen deposition in a transforming growth factor β1-driven precision cut lung slice (PCLS) model of pulmonary fibrosis (2016)
Journal Article
Brand, O. J., Pasini, A., Habgood, A., Knox, A. J., Jenkins, G., & Pang, L. (2016). Suberanilohydroxamic acid (SAHA) inhibits collagen deposition in a transforming growth factor β1-driven precision cut lung slice (PCLS) model of pulmonary fibrosis. Thorax, 71(Suppl. 3), A31. doi:10.1136/thoraxjnl-2016-209333.58

Introduction and Objectives: Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive interstitial lung disease that is refractory to current treatment options. Transforming growth factor (TGF)-β1 is a key pro-fibrotic cytokine that plays a cruc... Read More about Suberanilohydroxamic acid (SAHA) inhibits collagen deposition in a transforming growth factor β1-driven precision cut lung slice (PCLS) model of pulmonary fibrosis.

Loss of epithelial Gq and G11 signaling inhibits TGFβ production but promotes IL-33–mediated macrophage polarization and emphysema (2016)
Journal Article
John, A. E., Wilson, M. R., Habgood, A., Porte, J., Tatler, A. L., Stavrou, A., …Jenkins, R. G. (2016). Loss of epithelial Gq and G11 signaling inhibits TGFβ production but promotes IL-33–mediated macrophage polarization and emphysema. Science Signaling, 9(451), doi:10.1126/scisignal.aad5568

Heterotrimeric guanine nucleotide–binding protein (G protein) signaling is a ubiquitous signaling system that links hundreds of G protein–coupled receptors (GPCRs) with four G protein signaling pathways. Two of these pathways, one mediated by Gq and... Read More about Loss of epithelial Gq and G11 signaling inhibits TGFβ production but promotes IL-33–mediated macrophage polarization and emphysema.

First year of the thoracic triumvirate (2016)
Journal Article
Hart, N., Jenkins, G., & Smyth, A. R. (2016). First year of the thoracic triumvirate. Thorax, 71(7), 579-580. doi:10.1136/thoraxjnl-2016-208959

Secretory leukocyte protease inhibitor gene deletion alters bleomycin-induced lung injury, but not development of pulmonary fibrosis (2016)
Journal Article
Habgood, A., Tatler, A. L., Porte, J., Wahl, S. M., Laurent, G. J., John, A. E., …Jenkins, G. (in press). Secretory leukocyte protease inhibitor gene deletion alters bleomycin-induced lung injury, but not development of pulmonary fibrosis. Laboratory Investigation, https://doi.org/10.1038/labinvest.2016.40

Idiopathic pulmonary fibrosis is a progressive, fatal disease with limited treatment options. Protease-mediated transforming growth factor-β (TGF-β) activation has been proposed as a pathogenic mechanism of lung fibrosis. Protease activity in the lun... Read More about Secretory leukocyte protease inhibitor gene deletion alters bleomycin-induced lung injury, but not development of pulmonary fibrosis.

Caffeine inhibits TGFβ activation in epithelial cells, interrupts fibroblast responses to TGFβ, and reduces established fibrosis in ex vivo precision-cut lung slices (2016)
Journal Article
Tatler, A. L., Barnes, J., Habgood, A., Goodwin, A., McAnulty, R., & Jenkins, G. (2016). Caffeine inhibits TGFβ activation in epithelial cells, interrupts fibroblast responses to TGFβ, and reduces established fibrosis in ex vivo precision-cut lung slices. Thorax, 71(6), 565-567. doi:10.1136/thoraxjnl-2015-208215

Caffeine is a commonly used food additive found naturally in many products. In addition to potently stimulating the central nervous system caffeine is able to affect various systems within the body including the cardiovascular and respiratory systems... Read More about Caffeine inhibits TGFβ activation in epithelial cells, interrupts fibroblast responses to TGFβ, and reduces established fibrosis in ex vivo precision-cut lung slices.

Reduced Ets domain-containing protein Elk1 promotes pulmonary fibrosis via increased integrin αvβ6 expression (2016)
Journal Article
Tatler, A. L., Habgood, A., Porte, J., John, A. E., Stavrou, A., Hodge, E., …Jenkins, G. (2016). Reduced Ets domain-containing protein Elk1 promotes pulmonary fibrosis via increased integrin αvβ6 expression. Journal of Biological Chemistry, 291(18), 9540-9553. doi:10.1074/jbc.M115.692368

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease with high mortality. Active TGFβ1 is considered central to the pathogenesis of IPF. A major mechanism of TGFβ1 activation in the lung involves the epithelially restricted αvβ6... Read More about Reduced Ets domain-containing protein Elk1 promotes pulmonary fibrosis via increased integrin αvβ6 expression.