Dr Ling Chen
School of Biomedical Sciences and Pharmacy
- Phone:(02) 4921 1607
Dr Chen has a PhD in Biomedical Engineering from Chongqing University, China (2014) and a master in Sport Physiology from Chengdu Sports University, China (2010). While Dr Chen was working on her PhD degree, she had two years years PhD research training at Woolcock Institute of Medical Research, Sydney (2011-2013). During the two years training in Sydney, Dr Chen has gained her skills on primary lung cell culture and studied the mechanism of airway tissue remodelling in Chronic Obstructive Pulmonary Disease (COPD). Dr Chen started her professional career at the University of Tasmania as a Postdoctoral Research Fellow (2014-2017), where she has established her expertise in paediatric lung development and environmental effects on lung health. In July 2017, Dr Chen joined Hunter Medical Research Institute at the University of Newcastle, Australia and work with Laureate Professor Paul Foster and Dr Gerard Kaiko. Dr Chen’s research interests include investigating the pathophysiology of severe asthma, COPD and pulmonary fibrosis, and developing therapeutical approaches.
- PhD (Engineering), Chongqing University, China
- Airway remodelling
- Lung development
- Marridan (Maridan) (Mother)
- English (Fluent)
Fields of Research
|Title||Organisation / Department|
|Research Scientist||University of Newcastle
School of Biomedical Sciences and Pharmacy
|Research Scientist||University of Newcastle
School of Biomedical Sciences and Pharmacy
|Dates||Title||Organisation / Department|
|18/6/2014 - 30/6/2017||
Dr Ling Chen was a Postdoctoral Research Fellow at the School of Medicine in the faculty of healthy. Her reserach interests are focus on respiratory health and lung diseases.
|University of Tasmania
School of Medicine
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (18 outputs)
Wark PAB, Pathinayake PS, Kaiko G, Nichol K, Ali A, Chen L, et al., 'ACE2 expression is elevated in airway epithelial cells from older and male healthy individuals but reduced in asthma', Respirology, 26 442-451 (2021) [C1]
Background and objective: COVID-19 is complicated by acute lung injury, and death in some individuals. It is caused by SARS-CoV-2 that requires the ACE2 receptor and serine protea... [more]
Background and objective: COVID-19 is complicated by acute lung injury, and death in some individuals. It is caused by SARS-CoV-2 that requires the ACE2 receptor and serine proteases to enter AEC. We determined what factors are associated with ACE2 expression particularly in patients with asthma and COPD. Methods: We obtained lower AEC from 145 people from two independent cohorts, aged 2¿89 years, Newcastle (n = 115) and Perth (n = 30), Australia. The Newcastle cohort was enriched with people with asthma (n = 37) and COPD (n = 38). Gene expression for ACE2 and other genes potentially associated with SARS-CoV-2 cell entry was assessed by qPCR, and protein expression was confirmed with immunohistochemistry on endobronchial biopsies and cultured AEC. Results: Increased gene expression of ACE2 was associated with older age (P = 0.03) and male sex (P = 0.03), but not with pack-years smoked. When we compared gene expression between adults with asthma, COPD and healthy controls, mean ACE2 expression was lower in asthma patients (P = 0.01). Gene expression of furin, a protease that facilitates viral endocytosis, was also lower in patients with asthma (P = 0.02), while ADAM-17, a disintegrin that cleaves ACE2 from the surface, was increased (P = 0.02). ACE2 protein expression was also reduced in endobronchial biopsies from asthma patients. Conclusion: Increased ACE2 expression occurs in older people and males. Asthma patients have reduced expression. Altered ACE2 expression in the lower airway may be an important factor in virus tropism and may in part explain susceptibility factors and why asthma patients are not over-represented in those with COVID-19 complications.
Hoy R, Burdon J, Chen L, Miles S, Perret JL, Prasad S, et al., 'Work-related asthma: A position paper from the Thoracic Society of Australia and New Zealand and the National Asthma Council Australia', Respirology, 25 1183-1192 (2020) [C1]
Chen L, Bennett E, Wheeler AJ, Lyons AB, Woods GM, Johnston F, Zosky GR, 'Maternal exposure to particulate matter alters early post-natal lung function and immune cell development', Environmental Research, 164 625-635 (2018) [C1]
Background: In utero exposure to particulate matter (PM) from a range of sources is associated with adverse post-natal health; however, the effect of maternal exposure to communit... [more]
Background: In utero exposure to particulate matter (PM) from a range of sources is associated with adverse post-natal health; however, the effect of maternal exposure to community-sampled PM on early post-natal lung and immune development is poorly understood. Objectives: Using a mouse model, we aimed to determine whether in utero exposure to PM alters early post-natal lung function and immune cell populations. We used PM collected from ceiling voids in suburban houses as a proxy for community PM exposure. Methods: Pregnant C57BL/6 mice were intranasally exposed to ceiling derived PM, or saline alone, at gestational day (E) 13.5, 15.5, and 17.5. When mice were two weeks old, we assessed lung function by the forced oscillation technique, and enumerated T and B cell populations in the spleen and thymus by flow cytometry. Results: Maternal exposure to PM impaired somatic growth of male offspring resulting in reduced lung volume and deficits in lung function. There was no effect on thymic T cell populations in dams and their male offspring but PM decreased the CD4 +CD25 + T cell population in the female offspring. In contrast, maternal exposure to PM increased splenic CD3 +CD4 + and CD3 +CD8 + T cells in dams, and there was some evidence to suggest inhibition of splenic T cell maturation in male but not female offspring. Conclusions: Our findings suggested that maternal exposure to ceiling void PM has the capacity to impair early somatic growth and alter early life immune development in a sex specific manner.
Chen L, Wilson R, Bennett E, Zosky G, 'Identification Of Vitamin D Sensitive Pathways During Lung Development', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 193 (2016)
Chen L, Wilson R, Bennett E, Zosky GR, 'Identification of vitamin D sensitive pathways during lung development', RESPIRATORY RESEARCH, 17 (2016)
Ge Q, Chen L, Jaffar J, Argraves WS, Twal WO, Hansbro P, et al., 'Fibulin1C peptide induces cell attachment and extracellular matrix deposition in lung fibroblasts', SCIENTIFIC REPORTS, 5 (2015) [C1]
Chen L, Ge Q, Tjin G, Alkhouri H, Deng L, Brandsma CA, et al., 'Effects of cigarette smoke extract on human airway smooth muscle cells in COPD', European Respiratory Journal, 44 634-646 (2014)
We hypothesised that the response to cigarette smoke in airway smooth muscle (ASM) cells from smokers with chronic obstructive pulmonary disease (COPD) would be intrinsically diff... [more]
We hypothesised that the response to cigarette smoke in airway smooth muscle (ASM) cells from smokers with chronic obstructive pulmonary disease (COPD) would be intrinsically different from smokers without COPD, producing greater pro-inflammatory mediators and factors relating to airway remodelling. ASM cells were obtained from smokers with or without COPD, and then stimulated with cigarette smoke extract (CSE) or transforming growth factor-ß1. The production of chemokines and matrix metalloproteinases (MMPs) were measured by ELISA, and the deposition of collagens by extracellular matrix ELISA. The effects of CSE on cell attachment and wound healing were measured by toluidine blue attachment and cell tracker green wound healing assays. CSE increased the release of CXCL8 and CXCL1 from human ASM cells, and cells from smokers with COPD produced more CSE-induced CXCL1. The production of MMP-1, -3 and -10, and the deposition of collagen VIII alpha 1 (COL8A1) were increased by CSE, especially in the COPD group which had higher production of MMP-1 and deposition of COL8A1. CSE decreased ASM cell attachment and wound healing in the COPD group only. ASM cells from smokers with COPD were more sensitive to CSE stimulation, which may explain, in part, why some smokers develop COPD. Copyright ©ERS 2014.
Ojo O, Lagan AL, Rajendran V, Spanjer A, Chen L, Sohal SS, et al., 'Pathological changes in the COPD lung mesenchyme - Novel lessons learned from invitro and invivo studies', Pulmonary Pharmacology and Therapeutics, 29 121-128 (2014)
Chronic obstructive pulmonary disease (COPD) is currently the fourth leading cause of death worldwide and, in contrast to the trend for cardiovascular diseases, mortality rates st... [more]
Chronic obstructive pulmonary disease (COPD) is currently the fourth leading cause of death worldwide and, in contrast to the trend for cardiovascular diseases, mortality rates still continue to climb. This increase is in part due to an aging population, being expanded by the "Baby boomer" generation who grew up when smoking rates were at their peak and by people in developing countries living longer. Sadly, there has been a disheartening lack of new therapeutic approaches to counteract the progressive decline in lung function associated with the disease that leads to disability and death. COPD is characterized by irreversible chronic airflow limitation that is caused by emphysematous destruction of lung elastic tissue and/or obstruction in the small airways due to occlusion of their lumen by inflammatory mucus exudates, narrowing and obliteration. These lesions are mainly produced by the response of the tissue to the repetitive inhalational injury inflicted by noxious gases, including cigarette smoke, which involves interaction between infiltrating inflammatory immune cells, resident cells (e.g. epithelial cells and fibroblasts) and the extra cellular matrix. This interaction leads to tissue destruction and airway remodeling with changes in elastin and collagen, such that the epithelial-mesenchymal trophic unit is dysregulated in both the disease pathologies. This review focuses on: 1 - novel inflammatory and remodeling factors that are altered in COPD; 2 - invitro and invivo models to understand the mechanism whereby the extra cellular matrix environment in altered in COPD; and 3 - COPD in the context of wound-repair tissue responses, with a focus on the regulation of mesenchymal cell fate and phenotype.
Chen L, Perks KL, Stick SM, Kicic A, Larcombe AN, Zosky G, 'House Dust Mite Induced Lung Inflammation Does Not Alter Circulating Vitamin D Levels', PLOS ONE, 9 (2014)
Chen L, Ge Q, Black JL, Deng L, Burgess JK, Oliver BGG, 'Differential Regulation of Extracellular Matrix and Soluble Fibulin-1 Levels by TGF-beta(1) in Airway Smooth Muscle Cells', PLOS ONE, 8 (2013)
|Show 15 more journal articles|
Conference (14 outputs)
|2017||Chen L, Bennett E, Wheeler A, Johnston F, Zosky G, 'Effect Of In Utero Exposure To Ceiling Particles On Post-Natal Lung Function And Immune Cell Populations', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)|
|2017||Chen L, Bennett E, Wheeler A, Johnston F, Zosky G, 'EFFECT OF IN UTERO EXPOSURE TO CEILING PARTICLES ON POST-NATAL LUNG FUNCTION', RESPIROLOGY (2017)|
|2017||Chen L, Bennett E, Wheeler A, Johnston F, Zosky G, 'EFFECT OF IN UTERO EXPOSURE TO CEILING PARTICLES ON THE EARLY POST-NATAL IMMUNE CELL POPULATIONS', RESPIROLOGY (2017)|
|2016||Chen L, Wilson R, Bennett E, Zosky G, 'IMPACTS OF MATERNAL VITAMIN D DEFICIENCY ON LUNG DEVELOPMENT', RESPIROLOGY (2016)|
|2015||Chen L, Foong R, Bennett E, Zosky G, 'IN UTERO VITAMIN D DEFICIENCY ALTERS THE EXPRESSION OF MMP8 IN FOETAL LUNG', RESPIROLOGY, Queensland, AUSTRALIA (2015)|
|2014||Ge Q, Chen L, Jaffar J, Black JL, Burgess JK, Oliver BG, 'The Role Of Fibulin-1c Peptides In Attachment, Proliferation And Ecm Deposition In Lung Fibroblasts From Chronic Lung Diseases', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)|
Ge Q, Chen L, Jaffar J, Black J, Burgess J, Oliver B, 'FIBULIN-1C PEPTIDE INDUCES CELL ATTACHMENT, PROLIFERATION AND ECM DEPOSITION IN LUNG FIBROBLAST', RESPIROLOGY (2014)
|2013||Chen L, Ge Q, Black J, Burgess J, Oliver B, 'Cigarette smoke extract and TGF-beta(1) induce distinctive expression of extracellular matrix protein genes in human airway smooth muscle cells', EUROPEAN RESPIRATORY JOURNAL (2013)|
|2013||Chen L, Ge Q, Black JL, Burgess JK, Oliver BG, 'Difference Between Matrix And Soluble Fibulin-1 In Airway Smooth Muscle Cells', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)|
|2013||Ge Q, Jaffar J, Chen L, Black JL, Burgess JK, Oliver BG, 'Identification Of The Active Region Of Fibulin1 In Remodelling And Inflammation In Lung Fibroblasts', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)|
|2013||Chen L, Ge Q, Faiz A, Black JL, Burgess JK, Oliver BG, 'Cigarette Smoke Extract And Tgf-beta 1 Induce Distinctive Expression Of Extracellular Matrix And Adhesion Molecule Genes In COPD And Non-COPD Airway Smooth Muscle Cells', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)|
|2013||Chen L, Ge Q, Black JL, Burgess JK, Oliver BGG, 'DIFFERENCES BETWEEN DEPOSITED AND SOLUBLE FIBULIN-1 IN AIRWAY SMOOTH MUSCLE CELLS', RESPIROLOGY (2013)|
|2013||Ge Q, Jaffar J, Chen L, Black JL, Burgess JK, Oliver B, 'THE ROLE OF FIBULIN-1 PEPTIDES IN LUNG FIBROBLAST ASSOCIATED REMODELLING AND INFLAMMATION', RESPIROLOGY (2013)|
|Show 11 more conferences|
Grants and Funding
|Number of grants||1|
Click on a grant title below to expand the full details for that specific grant.
20181 grants / $26,000
Mini-organs in a dish: a personalised test for cystic fibrosis treatment to reduce the need for lung transplantation$26,000
Funding body: Hunter Medical Research Institute
The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.
|Country||Count of Publications|