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Effect of electronic cigarette extraction on vasoactive gene expression in human pulmonary artery smooth muscle and endothelial cells (2018)
Conference Proceeding
Alqarni, A., Brand, O., Pasini, A., Alshehri, M., & PANG, L. (2018). Effect of electronic cigarette extraction on vasoactive gene expression in human pulmonary artery smooth muscle and endothelial cells. doi:10.1136/thorax-2018-212555.61

Introduction Pulmonary Hypertension (PH) is a common and serious complication of COPD. We previously demonstrated that Cigarette Smoke Extracts (CSE) induced imbalanced vasoactive gene expression in human Pulmonary Artery Smooth Muscle Cells (hPASMCs... Read More

RAGE partially mediates cigarettes smoke extract induced cytokine and chemokine production in human bronchial epithelial cells (2018)
Journal Article
Alshehri, M., Brand, O., Alqarni, A., Pasini, A., & PANG, L. (2018). RAGE partially mediates cigarettes smoke extract induced cytokine and chemokine production in human bronchial epithelial cells. European Respiratory Journal, 52(Suppl. 62), doi:10.1183/13993003.congress-2018.PA4246

Chronic obstructive pulmonary disease (COPD) is a common inflammatory lung disease. Cigarette smoke (CS) is known to be the major cause of COPD. RAGE is a 35 kDa protein member belonging to the immunoglobulin superfamily of cell surface receptors. RA... Read More

The effect of cordycepin and simvastatin on cigarettes smoke extract induced cytokine and chemokine production in human bronchial epithelial cells (2018)
Journal Article
Alshehri, M., Brand, O., Alqarni, A., Pasini, A., & PANG, L. (2018). The effect of cordycepin and simvastatin on cigarettes smoke extract induced cytokine and chemokine production in human bronchial epithelial cells. European Respiratory Journal, 52(Suppl 62),

COPD is a common chronic inflammatory lung disease with cigarette smoke (CS) as the major cause. The receptor for advanced glycation end products (RAGE) and its ligands are critically involved in inflammation. Inhaled corticosteroids are poorly effec... Read More

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. ISSN 1044-1549

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

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. ISSN 0040-6376

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

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. ISSN 0040-6376

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