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
|060106||Cellular Interactions (incl. Adhesion, Matrix, Cell Wall)||20|
|100404||Regenerative Medicine (incl. Stem Cells and Tissue Engineering)||20|
|Title||Organisation / Department|
|Research Scientist||University of Newcastle
School of Biomedical Sciences and Pharmacy
|Dates||Title||Organisation / Department|
|18/06/2014 - 30/06/2017||
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For publications that are currently unpublished or in-press, details are shown in italics.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 (14 outputs)
Chen L, Zosky GR, 'Lung development', PHOTOCHEMICAL & PHOTOBIOLOGICAL SCIENCES, 16 339-346 (2017)
Chen L, Eapen M, Zosky G, 'Vitamin D both facilitates and attenuates the cellular response to lipopolysaccharide', Scientific Reports, 7 45172-45172 (2017)
NuÃ±ez NK, Bennett E, Chen L, Pitrez PM, Zosky GR, 'The independent effects of Vitamin D deficiency and house dust mite exposure on lung function are sex-specific', Scientific Reports, 7 (2017)
Â© 2017 The Author(s). Vitamin D deficiency is increasing around the world and has been associated with the development of asthma. This study aims to evaluate the effect of dietar... [more]
Â© 2017 The Author(s). Vitamin D deficiency is increasing around the world and has been associated with the development of asthma. This study aims to evaluate the effect of dietary vitamin D deficiency at different life stages on lung function using a murine model of allergic airways disease. BALB/c mice were challenged intranasally with HDM or saline alone for 10 days. Twenty four hours after the last challenge, mice were anesthetized and lung function was measured using the forced oscillation technique (FOT). Mice were euthanized for assessment of inflammation in the bronchoalveolar lavage (BAL) and total collagen content in lung homogenates by ELISA. Vitamin D deficiency impaired lung function in both male and female mice, increasing tissue damping and elastance, however had no effect on HDM induced inflammation. The impact of vitamin D deficiency was more evident in females. HDM also decreased airway distensibility, but only in females and this response was not altered by vitamin D deficiency. Our data suggest that vitamin D deficiency and HDM exposure have independent effects on lung mechanics and that females are more susceptible to these effects. Vitamin D deficiency may exacerbate lung function deficits by having a direct, but independent, effect on parenchymal mechanics.
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-Ã1. 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 Â©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)
Â© 2014 Elsevier Ltd. Chronic obstructive pulmonary disease (COPD) is currently the fourth leading cause of death worldwide and, in contrast to the trend for cardiovascular diseas... [more]
Â© 2014 Elsevier Ltd. 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 11 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)|
|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|
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|