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Imbalanced prostanoid release mediates cigarette smoke-induced human pulmonary artery cell proliferation (2022)
Journal Article
Alqarni, A. A., Brand, O. J., Pasini, A., Alahmari, M., Alghamdi, A., & Pang, L. (2022). Imbalanced prostanoid release mediates cigarette smoke-induced human pulmonary artery cell proliferation. Respiratory Research, 23(1), Article 136. https://doi.org/10.1186/s12931-022-02056-z

Background Pulmonary hypertension is a common and serious complication of chronic obstructive pulmonary disease (COPD). Studies suggest that cigarette smoke can initiate pulmonary vascular remodelling by stimulating cell proliferation; however, the... Read More about Imbalanced prostanoid release mediates cigarette smoke-induced human pulmonary artery cell proliferation.

S55 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). S55 Effect of electronic cigarette extraction on vasoactive gene expression in human pulmonary artery smooth muscle and endothelial cells. In Thorax: An International Journal of Respiratory Medicine - British Thoracic Society Winter Meeting 2018, 5 to 7 December 2018, Programme and Abstracts (Suppl 4: S55). https://doi.org/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 about S55 Effect of electronic cigarette extraction on vasoactive gene expression in human pulmonary artery smooth muscle and endothelial cells.

Effect of e-cigarette vapour extraction on vasoactive gene expression in human pulmonary artery smooth muscle and endothelial cells. (2018)
Journal Article
Alqarni, A., Brand, O., Pasini, A., Alshehri, M., & Pang, L. (2018). Effect of e-cigarette vapour extraction on vasoactive gene expression in human pulmonary artery smooth muscle and endothelial cells. European Respiratory Journal, 52(Suppl. 62), https://doi.org/10.1183/13993003.congress-2018.pa3110

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 (hPASMC... Read More about Effect of e-cigarette vapour extraction on vasoactive gene expression in human pulmonary artery smooth muscle and endothelial cells..

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 about RAGE partially mediates cigarettes smoke extract induced cytokine and chemokine production in human bronchial epithelial cells.

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), Article PA4245

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 about The effect of cordycepin and simvastatin on cigarettes smoke extract induced cytokine and chemokine production in human bronchial epithelial cells.

Suberanilohydroxamic acid prevents TGF-?1-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-?1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation. Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, 1861(5), https://doi.org/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-?1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation.

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, https://doi.org/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), Article A32. https://doi.org/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. https://doi.org/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 ?1-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 ?1-driven precision cut lung slice (PCLS) model of pulmonary fibrosis. Thorax, 71(Suppl. 3), A31. https://doi.org/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 ?1-driven precision cut lung slice (PCLS) model of pulmonary fibrosis.