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2. The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis

Author

Aghaei, Mahmoud, Dastghaib, Sanaz, Aftabi, Sajjad, Aghanoori, Mohamad-Reza, Alizadeh, Javad, Mokarram, Pooneh, Mehrbod, Parvaneh, Ashrafizadeh, Milad, Zarrabi, Ali, McAlinden, Kielan Darcy, Eapen, Mathew Suji, Sohal, Sukhwinder Singh, Sharma, Pawan, Zeki, Amir A, and Ghavami, Saeid

Subjects
Biochemistry and Cell Biology, Biological Sciences, Rare Diseases, Chronic Obstructive Pulmonary Disease, Lung, Autoimmune Disease, Aetiology, 2.1 Biological and endogenous factors, Respiratory, endoplasmic reticulum, fibrosis, tissue remodeling, non-coding RNA, UPR, autophagy, lung disease, Biochemistry and cell biology, Evolutionary biology, Applied computing
Abstract

Cellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the increased functional demands. Cells are able to induce a highly conserved adaptive mechanism, known as the unfolded protein response (UPR), to manage such stresses. UPR dysregulation and ER stress are involved in numerous human illnesses, such as metabolic syndrome, fibrotic diseases, and neurodegeneration, and cancer. Therefore, effective and specific compounds targeting the UPR pathway are being considered as potential therapies. This review focuses on the impact of both external and internal stressors on the ER in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) and discusses the role of the UPR signaling pathway activation in the control of cellular damage and specifically highlights the potential involvement of non-coding RNAs in COPD. Summaries of pathogenic mechanisms associated with the ER stress/UPR axis contributing to IPF and COPD, and promising pharmacological intervention strategies, are also presented.

Published
2021

3. Impact of Nebulized BromAc ® on Mucus Plug Clearance in a Mechanically Ventilated Ex Vivo Ovine Lung Model of Obstructive Respiratory Conditions.

Author

Valle, Nicole, Eapen, Mathew Suji, Pillai, Krishna, Morris, Richard, Akhter, Javed, Mekkawy, Ahmed H., Morris, David L., and Valle, Sarah J.

Subjects
*CHRONIC obstructive pulmonary disease, *AIRWAY resistance (Respiration), *ARTIFICIAL respiration, *BROMELIN, *CYSTIC fibrosis, *LUNGS
Abstract

Mucus plugging of the respiratory tract occurs in airway diseases, including asthma, chronic obstructive pulmonary disease, and cystic fibrosis. It can cause blockage of the airways, leading to breathlessness and lung failure. Here, we used a ventilatory setup to demonstrate the effect of BromAc® in dissolving mucus plugs in a novel ex vivo ovine obstructive lung model. Mucus simulant was filled into the trachea of freshly slaughtered ovine lungs and ventilated via an endotracheal tube (ETT) using Continuous Mandatory Ventilation. Predetermined single or repeated doses of Bromelain, Acetylcysteine (Ac), BromAc®, and saline control were administered via an Aerogen® vibrating nebulizer and ventilated for 30 or 60 min. Ventilatory recording of resistance, compliance, and tidal volume was conducted, and rheology pre- and post-treatment were measured. A significant decline in airway resistance (p < 0.0001) compared to the saline control was observed when treated with Bromelain, Ac, and BromAc®, with the latter showing a stronger mucolytic effect than single agents. The decline in resistance was also effective in shorter time points (p < 0.05) at lower doses of the drugs. Changes in compliance, peak pressure, and tidal volume were not observed after administration of the drugs. Rheology measurements revealed that BromAc®TM significantly reduced the viscosity of the mucin at the end of 30 min and 60 min time points (p < 0.001) compared to the saline control. BromAc® showed complete dissolution of the respiratory mucus simulant and improved ventilatory airflow parameters in the ex vivo ovine model. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Differential expression of mast cells in the small airways and alveolar septa of current smokers and patients with small airway disease and COPD

Author

Eapen, Mathew Suji, primary, Lu, Wenying, additional, Dey, Surajit, additional, Chia, Collin, additional, Hardikar, Ashutosh, additional, Hassan, Md Imtaiyaz, additional, Bhattarai, Prem, additional, Gaikwad, Archana Vijay, additional, Das, Shatarupa, additional, Hansbro, Philip M., additional, Singhera, Gurpreet Kaur, additional, Hackett, Tillie-Louise, additional, and Sohal, Sukhwinder Singh, additional

Published
2024
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6. Endothelial to mesenchymal transition is an active process in smokers and patients with early COPD contributing to pulmonary arterial pathology

Author

Bhattarai, Prem, primary, Lu, Wenying, additional, Hardikar, Ashutosh, additional, Dey, Surajit, additional, Gaikwad, Archana Vijay, additional, Shahzad, Affan Mahmood, additional, Chia, Collin, additional, Williams, Andrew, additional, Singhera, Gurpreet Kaur, additional, Hackett, Tillie-Louise, additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2023
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7. Taming the SARS-CoV-2-mediated proinflammatory response with BromAc®

Author

Ferreira, Geovane Marques, primary, Clarindo, Felipe Alves, additional, Ribeiro, Ágata Lopes, additional, Gomes-de-Pontes, Letícia, additional, de Carvalho, Luciana Debortoli, additional, Martins-Filho, Olindo Assis, additional, da Fonseca, Flávio Guimarães, additional, Teixeira, Mauro Martins, additional, Sabino, Adriano de Paula, additional, Eapen, Mathew Suji, additional, Morris, David L., additional, Valle, Sarah J., additional, and Coelho-dos-Reis, Jordana Grazziela Alves, additional

Published
2023
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9. Platelet Activating Factor Receptor and Intercellular Adhesion Molecule–1 Expression Increases in the Small Airway Epithelium and Parenchyma of Patients with Idiopathic Pulmonary Fibrosis: Implications for Microbial Pathogenesis.

Author

Shahzad, Affan Mahmood, Lu, Wenying, Dey, Surajit, Bhattarai, Prem, Gaikwad, Archana Vijay, Jaffar, Jade, Westall, Glen, Sutherland, Darren, Singhera, Gurpreet Kaur, Hackett, Tillie-Louise, Eapen, Mathew Suji, and Sohal, Sukhwinder Singh

Subjects
PLATELET activating factor, CELL adhesion, ALVEOLAR macrophages, EPITHELIUM, METHACHOLINE chloride, IMMUNOSTAINING, IDIOPATHIC pulmonary fibrosis
Abstract

Background: Idiopathic pulmonary fibrosis (IPF) is an irreversible lung fibrotic disorder of unknown cause. It has been reported that bacterial and viral co-infections exacerbate disease pathogenesis. These pathogens use adhesion molecules such as platelet activating factor receptor (PAFR) and intercellular adhesion molecule-1 (ICAM–1) to gain cellular entry, causing infections. Methods: Immunohistochemical staining was carried out for lung resections from IPF patients (n = 11) and normal controls (n = 12). The quantification of PAFR and ICAM–1 expression is presented as a percentage in the small airway epithelium. Also, type 2 pneumocytes and alveolar macrophages were counted as cells per mm2 of the parenchymal area and presented as a percentage. All image analysis was done using Image Pro Plus 7.0 software. Results: PAFR expression significantly increased in the small airway epithelium (p < 0.0001), type 2 pneumocytes (p < 0.0001) and alveolar macrophages (p < 0.0001) compared to normal controls. Similar trend was observed for ICAM–1 expression in the small airway epithelium (p < 0.0001), type 2 pneumocytes (p < 0.0001) and alveolar macrophages (p < 0.0001) compared to normal controls. Furthermore, the proportion of positively expressed type 2 pneumocytes and alveolar macrophages was higher in IPF than in normal control. Conclusions: This is the first study to show PAFR and ICAM–1 expression in small airway epithelium, type 2 pneumocytes and alveolar macrophages in IPF. These findings could help intervene microbial impact and facilitate management of disease pathogenesis. [ABSTRACT FROM AUTHOR]

Published
2024
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10. TGF-β1, pSmad-2/3, Smad-7, and β-Catenin Are Augmented in the Pulmonary Arteries from Patients with Idiopathic Pulmonary Fibrosis (IPF): Role in Driving Endothelial-to-Mesenchymal Transition (EndMT).

Author

Gaikwad, Archana Vijay, Eapen, Mathew Suji, Dey, Surajit, Bhattarai, Prem, Shahzad, Affan Mahmood, Chia, Collin, Jaffar, Jade, Westall, Glen, Sutherland, Darren, Singhera, Gurpreet Kaur, Hackett, Tillie-Louise, Lu, Wenying, and Sohal, Sukhwinder Singh

Subjects
*IDIOPATHIC pulmonary fibrosis, *PULMONARY artery, *VASCULAR remodeling, *WNT signal transduction, *CELLULAR signal transduction
Abstract

Background: We have previously reported that endothelial-to-mesenchymal transition (EndMT) is an active process in patients with idiopathic pulmonary fibrosis (IPF) contributing to arterial remodelling. Here, we aim to quantify drivers of EndMT in IPF patients compared to normal controls (NCs). Methods: Lung resections from thirteen IPF patients and eleven NCs were immunohistochemically stained for EndMT drivers, including TGF-β1, pSmad-2/3, Smad-7, and β-catenin. Intima, media, and adventitia were analysed for expression of each EndMT driver in pulmonary arteries. Computer- and microscope-assisted Image ProPlus7.0 image analysis software was used for quantifications. Results: Significant TGF-β1, pSmad-2/3, Smad-7, and β-catenin expression was apparent across all arterial sizes in IPF (p < 0.05). Intimal TGF-β1, pSmad-2/3, Smad-7, and β-catenin were augmented in the arterial range of 100–1000 μm (p < 0.001) compared to NC. Intimal TGF-β1 and β-catenin percentage expression showed a strong correlation with the percentage expression of intimal vimentin (r′ = 0.54, p = 0.05 and r′ = 0.61, p = 0.02, respectively) and intimal N-cadherin (r′ = 0.62, p = 0.03 and r′ = 0.70, p = 0.001, respectively). Intimal TGF-β1 and β-catenin expression were significantly correlated with increased intimal thickness as well (r′ = 0.52, p = 0.04; r′ = 0.052, p = 0.04, respectively). Moreover, intimal TGF-β1 expression was also significantly associated with increased intimal elastin deposition (r′ = 0.79, p = 0.002). Furthermore, total TGF-β1 expression significantly impacted the percentage of DLCO (r′ = −0.61, p = 0.03). Conclusions: This is the first study to illustrate the involvement of active TGF-β/Smad-2/3-dependent and β-catenin-dependent Wnt signalling pathways in driving EndMT and resultant pulmonary arterial remodelling in patients with IPF. EndMT is a potential therapeutic target for vascular remodelling and fibrosis in general in patients with IPF. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Profiling inflammatory cell populations in endobronchial biopsies from patients with asthma COPD overlap (ACO)

Author

Lu, Wenying, primary, Dey, Surajit, additional, Gaikwad, Archana Vijay, additional, Bhattarai, Prem, additional, Larby, Josie, additional, Chia, Collin, additional, Haug, Greg, additional, Weber, Heinrich C., additional, Young, Sally, additional, Pathinayake, Pabuddha S., additional, Wark, Peter A.B., additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2023
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13. TGF-β1, pSmad-2/3, Smad-7, and β-catenin are augmented in IPF pulmonary arteries: potential role in driving endothelial to mesenchymal transition (EndMT)

Author

Lu, Wenying, primary, Gaikwad, Archana Vijay, additional, Chia, Collin, additional, Larby, Josie, additional, Haug, Greg, additional, Dey, Surajit, additional, Bhattarai, Prem, additional, Jaffar, Jade, additional, Westall, Glen, additional, Singhera, Gurpreet Kaur, additional, Hackett, Tillie L., additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2023
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14. Chronic Obstructive Pulmonary Disease and Lung Cancer: Underlying Pathophysiology and New Therapeutic Modalities

Author

Eapen, Mathew Suji, Hansbro, Philip M., Larsson‑Callerfelt, Anna-Karin, Jolly, Mohit K., Myers, Stephen, Sharma, Pawan, Jones, Bernadette, Rahman, Md Atiqur, Markos, James, Chia, Collin, Larby, Josie, Haug, Greg, Hardikar, Ashutosh, Weber, Heinrich C., Mabeza, George, Cavalheri, Vinicius, Khor, Yet H., McDonald, Christine F., and Sohal, Sukhwinder Singh

Published
2018
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15. Transforming growth factor-β1 and SMAD signalling pathway in the small airways of smokers and patients with COPD: potential role in driving fibrotic type-2 epithelial mesenchymal transition

Author

Brake, Samuel James, primary, Lu, Wenying, additional, Chia, Collin, additional, Haug, Greg, additional, Larby, Josie, additional, Hardikar, Ashutosh, additional, Singhera, Gurpreet K., additional, Hackett, Tillie L., additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2023
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17. Endothelial-to-mesenchymal transition: a precursor to pulmonary arterial remodelling in patients with idiopathic pulmonary fibrosis

Author

Gaikwad, Archana Vijay, primary, Lu, Wenying, additional, Dey, Surajit, additional, Bhattarai, Prem, additional, Haug, Greg, additional, Larby, Josie, additional, Chia, Collin, additional, Jaffar, Jade, additional, Westall, Glen, additional, Singhera, Gurpreet Kaur, additional, Hackett, Tillie-Louise, additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2023
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18. SARS-CoV-2 (COVID-19) Adhesion Site Protein Upregulation in Small Airways, Type 2 Pneumocytes, and Alveolar Macrophages of Smokers and COPD – Possible Implications for Interstitial Fibrosis

Author

Brake, Samuel James, Eapen, Mathew Suji, McAlinden, Kielan Darcy, Markos, James, Haug, Greg, Larby, Josie, Chia, Collin, Hardikar, Ashutosh, Singhera, Gurpreet Kaur, Hackett, Tillie L, Lu, Wenying, and Sohal, Sukhwinder Singh

Subjects
Smokers, SARS-CoV-2, COVID-19, ACE2, alveolar macrophages, General Medicine, International Journal of Chronic Obstructive Pulmonary Disease, Fibrosis, smoking, respiratory tract diseases, Up-Regulation, Pulmonary Disease, Chronic Obstructive, Cross-Sectional Studies, Alveolar Epithelial Cells, Macrophages, Alveolar, COPD, type 2 pneumocytes, Humans, epithelium, Original Research
Abstract

Samuel James Brake,1 Mathew Suji Eapen,1 Kielan Darcy McAlinden,1 James Markos,1,2 Greg Haug,1,2 Josie Larby,1,2 Collin Chia,1,2 Ashutosh Hardikar,1,3 Gurpreet Kaur Singhera,4,5 Tillie L Hackett,4,5 Wenying Lu,1 Sukhwinder Singh Sohal1 1Respiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, College of Health and Medicine, University of Tasmania, Launceston, TAS, 7248, Australia; 2Department of Respiratory Medicine, Launceston General Hospital, Launceston, TAS, 7250, Australia; 3Department of Cardiothoracic Surgery, Royal Hobart Hospital, Hobart, TAS, 7000, Australia; 4Department of Anesthesiology, Pharmacology, and Therapeutics, University of British Columbia, Vancouver, BC, Canada; 5Department of Medicine, University of British Columbia Centre for Heart Lung Innovation, St. Paul’s Hospital, Vancouver, BC, CanadaCorrespondence: Sukhwinder Singh SohalRespiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, College of Health and Medicine, University of Tasmania, Locked Bag – 1322, Newnham Drive, Launceston, TAS, 7248, AustraliaTel +61 3 6324 5434Email sssohal@utas.edu.auBackground: Smokers and patients with COPD are highly susceptible to SARS-CoV-2 infection, leading to severe COVID-19.Methods: This cross-sectional study involved resected lung tissues from 16 patients with GOLD stage I or II COPD; of which 8 were current smokers COPD (COPD-CS), and 8 ex-smokers COPD (COPD-ES), 7 normal lung function smokers (NLFS), 9 patients with small airways disease (SAD), and 10 were never-smoking normal controls (NC). Immunostaining for ACE2, Furin, and TMPRSS2 was performed and analysed for percent expression in small airway epithelium (SAE) and counts for positively and negatively stained type 2 pneumocytes and alveolar macrophages (AMs) were done using Image ProPlus V7.0. Furthermore, primary small airway epithelial cells (pSAEC) were analysed by immunofluorescence after exposure to cigarette smoke extract (CSE).Results: ACE2, Furin, and TMPRSS2 expression significantly increased in SAE and type 2 pneumocytes in all the subjects (except Furin for NLFS) compared to NC (p < 0.001). Similar significance was observed for ACE2 positive AM (p < 0.002), except COPD-ES, which decreased in ACE2 positive AMs (p < 0.003). Total type 2 pneumocytes and AMs significantly increased in the pathological groups compared to NC (p < 0.01), except SAD (p = 0.08). However, AMs are significantly reduced in COPD-ES (p < 0.003). Significant changes were observed for tissue co-expression of Furin and TMPRSS2 with ACE2 in SAE, type 2 pneumocytes and AMs. These markers also negatively correlated with lung function parameters, such as FEV1/FVC % predicted, FEF25-75%, DLCO% predicted. A strong co-localisation and expression for ACE2 (p < 0.0001), Furin (p < 0.01), and TMPRSS2 (p < 0.0001) was observed in pSAEC treated with 1% CSE than controls.Discussion: The increased expression of ACE2, TMPRSS2 and Furin, in the SAE, type 2 pneumocytes and AMs of smokers and COPD are detrimental to lung function and proves that these patient groups could be more susceptible to severe COVID-19 infection. Increased type 2 pneumocytes suggest that these patients are vulnerable to developing post-COVID-19 interstitial pulmonary fibrosis or fibrosis in general. There could be a silently developing interstitial pathology in smokers and patients with COPD. This is the first comprehensive study to report such changes.Keywords: COVID-19, SARS-CoV-2, smoking, COPD, ACE2, type 2 pneumocytes, alveolar macrophages, epithelium

Published
2022

19. Differential airway remodeling changes were observed in patients with asthma COPD overlap compared to patients with asthma and COPD alone

Author

Dey, Surajit, primary, Lu, Wenying, additional, Weber, Heinrich C., additional, Young, Sally, additional, Larby, Josie, additional, Chia, Collin, additional, Haug, Greg, additional, Brake, Samuel James, additional, Myers, Stephen, additional, Gaikwad, Archana Vijay, additional, Bhattarai, Prem, additional, Pathinayake, Prabuddha S., additional, Wark, Peter A. B., additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2022
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20. Arterial remodelling in smokers and in patients with small airway disease and COPD: implications for lung physiology and early origins of pulmonary hypertension

Author

Bhattarai, Prem, primary, Lu, Wenying, additional, Gaikwad, Archana Vijay, additional, Dey, Surajit, additional, Chia, Collin, additional, Larby, Josie, additional, Haug, Greg, additional, Hardikar, Ashutosh, additional, Williams, Andrew, additional, Kaur Singhera, Gurpreet, additional, Hackett, Tillie-Louise, additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2022
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21. SARS-CoV-2 (COVID-19) Adhesion Site Protein Upregulation in Small Airways, Type 2 Pneumocytes, and Alveolar Macrophages of Smokers and COPD – Possible Implications for Interstitial Fibrosis

Author

Brake,Samuel James, Eapen,Mathew Suji, McAlinden,Kielan Darcy, Markos,James, Haug,Greg, Larby,Josie, Chia,Collin, Hardikar,Ashutosh, Singhera,Gurpreet Kaur, Hackett,Tillie L, Lu,Wenying, Sohal,Sukhwinder Singh, Brake,Samuel James, Eapen,Mathew Suji, McAlinden,Kielan Darcy, Markos,James, Haug,Greg, Larby,Josie, Chia,Collin, Hardikar,Ashutosh, Singhera,Gurpreet Kaur, Hackett,Tillie L, Lu,Wenying, and Sohal,Sukhwinder Singh

Abstract

Samuel James Brake,1 Mathew Suji Eapen,1 Kielan Darcy McAlinden,1 James Markos,1,2 Greg Haug,1,2 Josie Larby,1,2 Collin Chia,1,2 Ashutosh Hardikar,1,3 Gurpreet Kaur Singhera,4,5 Tillie L Hackett,4,5 Wenying Lu,1 Sukhwinder Singh Sohal1 1Respiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, College of Health and Medicine, University of Tasmania, Launceston, TAS, 7248, Australia; 2Department of Respiratory Medicine, Launceston General Hospital, Launceston, TAS, 7250, Australia; 3Department of Cardiothoracic Surgery, Royal Hobart Hospital, Hobart, TAS, 7000, Australia; 4Department of Anesthesiology, Pharmacology, and Therapeutics, University of British Columbia, Vancouver, BC, Canada; 5Department of Medicine, University of British Columbia Centre for Heart Lung Innovation, St. Paul’s Hospital, Vancouver, BC, CanadaCorrespondence: Sukhwinder Singh SohalRespiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, College of Health and Medicine, University of Tasmania, Locked Bag – 1322, Newnham Drive, Launceston, TAS, 7248, AustraliaTel +61 3 6324 5434Email sssohal@utas.edu.auBackground: Smokers and patients with COPD are highly susceptible to SARS-CoV-2 infection, leading to severe COVID-19.Methods: This cross-sectional study involved resected lung tissues from 16 patients with GOLD stage I or II COPD; of which 8 were current smokers COPD (COPD-CS), and 8 ex-smokers COPD (COPD-ES), 7 normal lung function smokers (NLFS), 9 patients with small airways disease (SAD), and 10 were never-smoking normal controls (NC). Immunostaining for ACE2, Furin, and TMPRSS2 was performed and analysed for percent expression in small airway epithelium (SAE) and counts for positively and negatively stained type 2 pneumocytes and alveolar macrophages (AMs) were done using Image ProPlus V7.0. Furthermore, primary small airway epithelial cells (pSAEC) were analysed by immunofluorescence after exposu

Published
2022

24. Vascular remodelling in IPF patients and its detrimental effect on lung physiology: potential role of endothelial to mesenchymal transition (EndMT)

Author

Gaikwad, Archana Vijay, primary, Lu, Wenying, additional, Dey, Surajit, additional, Bhattarai, Prem, additional, Chia, Collin, additional, Larby, Josie, additional, Haug, Greg, additional, Myers, Stephen, additional, Jaffar, Jade, additional, Westall, Glen, additional, Singhera, Gurpreet Kaur, additional, Hackett, Tillie-Louise, additional, Markos, James, additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2022
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25. Angiotensin-Converting Enzyme 2 (ACE2), Transmembrane Peptidase Serine 2 (TMPRSS2), and Furin Expression Increases in the Lungs of Patients with Idiopathic Pulmonary Fibrosis (IPF) and Lymphangioleiomyomatosis (LAM): Implications for SARS-CoV-2 (COVID-19) Infections

Author

Lu, Wenying, primary, Eapen, Mathew Suji, additional, Singhera, Gurpreet Kaur, additional, Markos, James, additional, Haug, Greg, additional, Chia, Collin, additional, Larby, Josie, additional, Brake, Samuel James, additional, Westall, Glen P., additional, Jaffar, Jade, additional, Kalidhindi, Rama Satyanarayana Raju, additional, Fonseka, Nimesha De, additional, Sathish, Venkatachalem, additional, Hackett, Tillie L., additional, and Sohal, Sukhwinder Singh, additional

Published
2022
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28. Anti-Inflammatory Activity of Fucoidan Extracts In Vitro

Author

Ahmad, Tauseef, primary, Eapen, Mathew Suji, additional, Ishaq, Muhammad, additional, Park, Ah Young, additional, Karpiniec, Samuel S., additional, Stringer, Damien N., additional, Sohal, Sukhwinder Singh, additional, Fitton, J. Helen, additional, Guven, Nuri, additional, Caruso, Vanni, additional, and Eri, Rajaraman, additional

Published
2021
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30. Impact of Deleterious Mutations on Structure, Function and Stability of Serum/Glucocorticoid Regulated Kinase 1: A Gene to Diseases Correlation

Author

AlAjmi, Mohamed F., primary, Khan, Shama, additional, Choudhury, Arunabh, additional, Mohammad, Taj, additional, Noor, Saba, additional, Hussain, Afzal, additional, Lu, Wenying, additional, Eapen, Mathew Suji, additional, Chimankar, Vrushali, additional, Hansbro, Philip M, additional, Sohal, Sukhwinder Singh, additional, Elasbali, Abdelbaset Mohamed, additional, and Hassan, Md. Imtaiyaz, additional

Published
2021
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31. Increased arterial remodelling in smokers and mild-moderate COPD patients are indicative of potential early onset of pulmonary hypertension

Author

Bhattarai, Prem, primary, Lu, Wenying, additional, Markos, James, additional, Chia, Collin, additional, Larby, Josie, additional, Haug, Greg, additional, Williams, Andrew, additional, Myers, Stephen, additional, Hardikar, Ashutosh, additional, Gaikwad, Archana Vijay, additional, Dey, Surajit, additional, Singhera, Gurpreet Kaur, additional, Hackett, Tillie L., additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2021
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32. Airway remodelling augmented in patients with asthma COPD overlap (ACO) compared to asthma and COPD

Author

Dey, Surajit, primary, Lu, Wenying, additional, Markos, James, additional, Larby, Josie, additional, Chia, Collin, additional, Haug, Greg, additional, Weber, Heinrich C., additional, Brake, Samuel James, additional, Myers, Stephen, additional, Gaikwad, Archana Vijay, additional, Bhattarai, Prem, additional, Wark, Peter A.B, additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2021
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33. Arterial remodelling in patients with idiopathic pulmonary fibrosis (IPF) and the possible role of endothelial to mesenchymal transition (EndMT)

Author

Gaikwad, Archana Vijay, primary, Lu, Wenying, additional, Dey, Surajit, additional, Bhattarai, Prem, additional, Chia, Collin, additional, Larby, Josie, additional, Haug, Greg, additional, Myers, Stephen, additional, Brake, Samuel James, additional, Jaffar, Jade, additional, Westall, Glen Philip, additional, Singhera, Gurpreet Kaur, additional, Hackett, Tillie-Louise, additional, Markos, James, additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2021
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34. Increased expression of SARS-CoV-2 (Covid-19) adhesion sites on type II pneumocytes, small airway epithelium, and alveolar macrophages in smokers and patients with COPD

Author

Brake, Samuel James, primary, Lu, Wenying, additional, Markos, James, additional, Larby, Josie, additional, Chia, Collin, additional, Haug, Greg, additional, Weber, Heinrich C., additional, Mcalinden, Kielan Darcy, additional, Hardikar, Ashutosh, additional, Singhera, Gurpreet Kaur, additional, Hackett, Tillie L., additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2021
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39. Increased myofibroblasts in the small airways, and relationship to remodelling and functional changes in smokers and COPD patients: potential role of epithelial–mesenchymal transition

Author

Eapen, Mathew Suji, Lu, Wenying, Hackett, Tillie L, Singhera, Gupreet Kaur, Mahmood, Malik Quasir, Hardikar, Ashutosh, Ward, Chris, Walters, Eugene H, Sohal, Sukhwinder Singh, Eapen, Mathew Suji, Lu, Wenying, Hackett, Tillie L, Singhera, Gupreet Kaur, Mahmood, Malik Quasir, Hardikar, Ashutosh, Ward, Chris, Walters, Eugene H, and Sohal, Sukhwinder Singh

Abstract

Introduction Previous reports have shown epithelial–mesenchymal transition (EMT) as an active process that contributes to small airway fibrotic pathology. Myofibroblasts are highly active pro-fibrotic cells that secrete excessive and altered extracellular matrix (ECM). Here we relate small airway myofibroblast presence with airway remodelling, physiology and EMT activity in smokers and COPD patients. Methods Lung resections from nonsmoker controls, normal lung function smokers and COPD current and ex-smokers were stained with anti-human α-smooth muscle actin (SMA), collagen 1 and fibronectin. αSMA+ cells were computed in reticular basement membrane (Rbm), lamina propria and adventitia and presented per mm of Rbm and mm2 of lamina propria. Collagen-1 and fibronectin are presented as a percentage change from normal. All analyses including airway thickness were measured using Image-pro-plus 7.0. Results We found an increase in subepithelial lamina propria (especially) and adventitia thickness in all pathological groups compared to nonsmoker controls. Increases in αSMA+ myofibroblasts were observed in subepithelial Rbm, lamina propria and adventitia in both the smoker and COPD groups compared to nonsmoker controls. Furthermore, the increase in the myofibroblast population in the lamina propria was strongly associated with decrease in lung function, lamina propria thickening, increase in ECM protein deposition, and finally EMT activity in epithelial cells. Conclusions This is the first systematic characterisation of small airway myofibroblasts in COPD based on their localisation, with statistically significant correlations between them and other pan-airway structural, lung function and ECM protein changes. Finally, we suggest that EMT may be involved in such changes.

Published
2021

40. Increased myofibroblasts in the small airways, and relationship to remodelling and functional changes in smokers and COPD patients: potential role of epithelial–mesenchymal transition

Author

Eapen, Mathew Suji, primary, Lu, Wenying, additional, Hackett, Tillie L., additional, Singhera, Gurpreet Kaur, additional, Mahmood, Malik Q., additional, Hardikar, Ashutosh, additional, Ward, Chris, additional, Walters, Eugene Haydn, additional, and Sohal, Sukhwinder Singh, additional

Published
2021
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41. Electronic Cigarette Aerosol Is Cytotoxic and Increases ACE2 Expression on Human Airway Epithelial Cells: Implications for SARS-CoV-2 (COVID-19)

Author

McAlinden, Kielan Darcy, primary, Lu, Wenying, additional, Ferdowsi, Parisa Vahidi, additional, Myers, Stephen, additional, Markos, James, additional, Larby, Josie, additional, Chia, Collin, additional, Weber, Heinrich C., additional, Haug, Greg, additional, Eapen, Mathew Suji, additional, and Sohal, Sukhwinder Singh, additional

Published
2021
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42. Endothelial to mesenchymal transition (EndMT): a precursor to post-SARS-CoV-2 infection (COVID-19) interstitial pulmonary fibrosis and vascular obliteration?

Author

Eapen, Mathew Suji, Lu, Wenying, Gaikwad, Archana Vijay, Bhattarai, Prem, Chia, Collin, Hardikar, Ashutosh, Haug, Greg, and Sohal, Sukhwinder Singh

Subjects
Betacoronavirus, Intensive Care Units, SARS-CoV-2, Correspondence, Pneumonia, Viral, COVID-19, Endothelial Cells, Humans, Venous Thromboembolism, Coronavirus Infections, Pandemics
Abstract

We read with interest the recent editorial by Huertas and colleagues, highlighting the importance of endothelial cell dysfunction in patients with SARS-CoV-2 (COVID-19) infection [1]. The authors have made some very fascinating insights, and we would like to take this discussion further, especially emphasising the role of endothelial cells in initiating post-infection pulmonary fibrosis and vascular remodelling. The angiotensin-converting-enzyme-2 (ACE2) has been suggested as the primary receptor for mediating SARS-CoV-2 entry into the host cells. Apart from ACE2, the other key players that facilitate the SARS-CoV-2 entry, includes transmembrane serine protease 2 (TMPRSS2), furin, sialic acid and the extracellular matrix metalloproteinase inducer (CD147) [1]. In the article, authors provide compelling comprehensions from a study comparing post-mortem lung tissues from patients who died from COVID-19 with acute respiratory distress syndrome due to influenza A (H1N1) infection and those with age-matched, uninfected control lungs [1, 2]. A crucial inference was the connections between the significant increase in ACE2 positive endothelial cells and the substantial change in endothelial cell morphology, disruption of intercellular junctions, cell swelling, and the breakdown of the underlying basement membrane, all indicative of vascular structural modification in tune to the process of endothelial to mesenchymal transition (EndMT) [3]. Considering the implications for post-COVID-19 pulmonary fibrosis and vascular destruction seen in this infectious pathology, we believe that the role of EndMT in disease manifestation could be consequential., Endothelial to mesenchymal transition (EndMT) could lead to post-COVID-19 pulmonary fibrosis and vascular remodelling.

Published
2020

43. Dysregulation of endocytic machinery and ACE2 in small airways of smokers and COPD patients can augment their susceptibility to SARS-CoV-2 (COVID-19) infections

Author

Eapen, Mathew Suji, primary, Lu, Wenying, additional, Hackett, Tillie L., additional, Singhera, Gurpreet Kaur, additional, Thompson, Isobel E., additional, McAlinden, Kielan Darcy, additional, Hardikar, Ashutosh, additional, Weber, Heinrich C., additional, Haug, Greg, additional, Wark, Peter A. B., additional, Chia, Collin, additional, and Sohal, Sukhwinder Singh, additional

Published
2021
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44. The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis

Author

Aghaei, Mahmoud, primary, Dastghaib, Sanaz, additional, Aftabi, Sajjad, additional, Aghanoori, Mohamad-Reza, additional, Alizadeh, Javad, additional, Mokarram, Pooneh, additional, Mehrbod, Parvaneh, additional, Ashrafizadeh, Milad, additional, Zarrabi, Ali, additional, McAlinden, Kielan Darcy, additional, Eapen, Mathew Suji, additional, Sohal, Sukhwinder Singh, additional, Sharma, Pawan, additional, Zeki, Amir A., additional, and Ghavami, Saeid, additional

Published
2020
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46. Expression of microRNAs following radiation therapy and association with severity of radiotherapy‑induced toxicity among patients with prostate adenocarcinoma: A systematic review and meta‑analysis.

Author

Singh, Jagtar, Thachil, Thanuja, Misir, Sema, Altay, Diler Us, Yaman, Serap Ozer, Singh, Gurpreet, Eapen, Mathew Suji, McAlinden, Kielan Darcy, Petrovic, Nina, and Sohal, Sukhwinder Singh

Subjects
GENE expression, PROGRESSION-free survival, META-analysis, MONONUCLEAR leukocytes, RADIOTHERAPY, LUTEINIZING hormone releasing hormone, MICRORNA, PROSTATE
Abstract

Radiation-induced normal tissue toxicity is a common acute and chronic outcome of radiotherapy (RT) for prostate cancer (PCa). There are currently no existing pre-assessments before treatment to predict acute and late RT-induced toxicity. Novel predictive blood biomarkers in radiation oncology may improve treatment decision-making and therapeutic monitoring for patients with PCa. A comprehensive systematic search of microRNA (miRNA/miR) profiling studies published in PubMed, Science Direct and Google Scholar was performed. The present systematic review, supported by meta-analysis, summarises key findings and discusses the results of prospective clinical studies investigating miRNA expression levels and their association with RT-induced toxicity in PCa. Out of seven clinical studies, six highlighted levels of 10 miRNAs changing in plasma, serum or peripheral blood mononuclear cells during RT. The post-RT expression levels of miRNA-132-5p, miRNA-1-3p, miRNA-410 and miRNA-221 were increased, and miRNA-23a-3p expression was decreased among patients with low-grade RT-induced toxicity. Furthermore, in patients with high-grade RT toxicity, miRNA-197-3p, miRNA-151a-5p, miRNA-18b-5p, miRNA-99a and miRNA-21 expression was increased, while miRNA-132-5p expression was decreased. The present miRNA meta-analysis could be the focus of future studies to identify their potential clinical value as PCa biomarkers and therapeutic mediators in RT-induced toxicity. The variations in miRNA levels post-RT could be used as predictive biomarkers of RT-induced toxicity. However, further extensive validation is required to establish the relationship between miRNA expression levels and RT-induced toxicity in PCa and to confirm their predictive value. [ABSTRACT FROM AUTHOR]

Published
2024
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