e-learning
resources
Munich 2014
Tuesday, 09.09.2014
Cell biology 2014
Login
Search all ERS
e-learning
resources
Disease Areas
Airways Diseases
Interstitial Lung Diseases
Respiratory Critical Care
Respiratory Infections
Paediatric Respiratory Diseases
Pulmonary Vascular Diseases
Sleep and Breathing Disorders
Thoracic Oncology
Events
International Congress
Courses
Webinars
Conferences
Research Seminars
Journal Clubs
Publications
Breathe
Monograph
ERJ
ERJ Open Research
ERR
European Lung White Book
Handbook Series
Guidelines
All ERS guidelines
e-learning
CME Online
Case reports
Short Videos
SpirXpert
Procedure Videos
CME tests
Reference Database of Respiratory Sounds
Radiology Image Challenge
Brief tobacco interventions
EU Projects
VALUE-Dx
ERN-LUNG
ECRAID
UNITE4TB
Disease Areas
Events
Publications
Guidelines
e-learning
EU Projects
Login
Search
Mitochondrial reactive oxygen species (ROS) mediate proliferation and cytokine release in airway smooth muscle cells of patients with COPD
C. Michaeloudes, C. Wiegman, P. Kirkham, K. F. Chung, I. Adcock, COPD MAP Consortium WP3 (London, United Kingdom)
Source:
International Congress 2014 – Cell biology 2014
Session:
Cell biology 2014
Session type:
Thematic Poster Session
Number:
3845
Disease area:
Airway diseases
Abstract
Background: The inflammatory response in COPD is accompanied by small airway remodelling, with increased airway smooth muscle (ASM) mass, as a result of ASM cell (ASMC) hyperplasia. Oxidative stress, a key mediator of inflammation and remodelling in COPD, triggers mitochondrial dysfunction and increased ROS levels in ASMCs from healthy subjects. Mitochondrial ROS release is more pronounced in ASMCs from patients with COPD suggesting an inherent mitochondrial dysfunction. We hypothesised that mitochondrial ROS may trigger the hyperproliferative ASMC phenotype observed in COPD. Aims and Objectives: The role of mitochondrial ROS in mediating proliferation and inflammatory mediator release from ASMCs of patients with COPD was investigated. Methods: ASMCs were isolated from bronchoscopic biopsies of healthy non-smokers and patients with COPD. Cell proliferation was measured as rate of BrdU incorporation and total cellular DNA. The role of mitochondrial ROS was studied using the mitochondria-targeted antioxidant MitoQ (1µM) and the mitochondria-permeable antioxidant Tiron (0.1-10mM). Results: Foetal bovine serum (FBS; 2.5%) and TGF-
b
(1ng/mL) increased the proliferation of ASMCs from healthy subjects (
~
30-fold; p<0.001) and patients with COPD (
~
40-fold; p<0.001). FBS and TGF-
b
-induced proliferation of ASMCs, from both groups, was reduced by pre-treatment with MitoQ (
~
50%; p<0.05) or Tiron (
~
80%; p<0.01). MitoQ also partially inhibited TNF-
a
(0.1ng/ml)-induced IL-8 release in ASMCs from both groups. Conclusion: Mitochondrial oxidative stress may be an interesting target for preventing ASMC hyperproliferation in COPD.
Rating:
You must
login
to grade this presentation.
Share or cite this content
Citations should be made in the following way:
C. Michaeloudes, C. Wiegman, P. Kirkham, K. F. Chung, I. Adcock, COPD MAP Consortium WP3 (London, United Kingdom). Mitochondrial reactive oxygen species (ROS) mediate proliferation and cytokine release in airway smooth muscle cells of patients with COPD. Eur Respir J 2014; 44: Suppl. 58, 3845
You must
login
to share this Presentation/Article on Twitter, Facebook, LinkedIn or by email.
Member's Comments
No comment yet.
You must
Login
to comment this presentation.
Related content which might interest you:
Late Breaking Abstract - Implications of treatable traits and treatment choices on exacerbation risk in moderate-severe asthma
Impact of Dexamethasone on pathogen profile of COVID-19 patients requiring intensive care: a multicentre retrospective study
Muscle energy techniques for COPD patients: Effects on pulmonary function and activities of daily living
Related content which might interest you:
Mitochondrial reactive oxygen species and glycolysis in airway smooth muscle cell proliferation in COPD
Source: International Congress 2015 – Advances in the future treatment of COPD
Year: 2015
Effect of oxidative stress on mitochondrial function in airway smooth muscle (ASM) cells from COPD patients
Source: Annual Congress 2013 –Airway smooth muscle and cell biology
Year: 2013
Mitochondrial membrane potential in the airway and skeletal muscle compartments of smokers with and without COPD
Source: International Congress 2014 – Translational studies in COPD
Year: 2014
CCL2 release by airway smooth muscle is increased in asthma and promotes fibrocyte migration
Source: International Congress 2014 – Cell biology 2014
Year: 2014
MNK-1 inhibition reduces proliferation and CXCL10 in airway smooth muscle cells
Source: Annual Congress 2013 –Airway smooth muscle and cell biology
Year: 2013
Secretion of hyaluronic acid is mediated by muscarinic receptors in airway smooth muscle cells of patients with COPD
Source: International Congress 2014 – Translational studies in COPD
Year: 2014
Targeting ASK1 in preventing airway smooth muscle growth: Implications for airway remodeling in COPD
Source: International Congress 2016 – New findings in mucosal immunology
Year: 2016
Hypoxia exerts dualistic effects on inflammatory and proliferative responses of healthy and asthmatic primary human bronchial smooth muscle cells
Source: International Congress 2014 – Cell biology 2014
Year: 2014
Plasminogen-stimulated inflammatory cytokine production by airway smooth muscle cells is regulated by annexin A2
Source: Annual Congress 2013 –Airway smooth muscle and cell biology
Year: 2013
Corticosteroid insensitivity in airway smooth muscle cells from severe asthma is dependent on stimulus and cytokine product
Source: International Congress 2014 – Cell biology 2014
Year: 2014
p53 dysfunction increased mitochondrial biogenesis and bronchial smooth muscle cell proliferation in asthma
Source: International Congress 2015 – Airway remodelling: recent developments
Year: 2015
Altered mitochondrial reactive oxygen species (ROS) production in airway smooth muscle cells of severe asthma.
Source: International Congress 2019 – Novel mechanisms elucidated by translational studies of asthma
Year: 2019
The anti-proliferative effect of hydrogen sulfide upon human airway smooth muscle in COPD
Source: International Congress 2014 – New drugs for asthma, COPD and pulmonary fibrosis
Year: 2014
Link between airway inflammation and remodeling: TNFα induces airway smooth muscle cell proliferation via an ET1/GMCSF/IL6 network
Source: International Congress 2015 – Airway remodelling: recent developments
Year: 2015
Airway smooth muscle contractility is increased following coculture with fibrocytes
Source: International Congress 2016 – Mechanisms of disease
Year: 2016
Integrins regulate eosinophil adhesion to the airway smooth muscle cells in asthma patients
Source: International Congress 2015 – Asthma mechanisms and management
Year: 2015
Impaired inhibitory action of corticosteroids on chemokine expression induced by TNFalpha in airway smooth muscle (ASM) cells from patients with severe asthma
Source: Annual Congress 2013 –Airway smooth muscle and cell biology
Year: 2013
DP2/CRTh2 is expressed by ASM cells in asthma and its inhibition suppresses ASM migration
Source: International Congress 2016 – Mechanisms of disease
Year: 2016
Investigating mitochondrial dysfunction in asthma
Source: International Congress 2015 – Advances in the future treatment of severe asthma
Year: 2015
Extracellular matrix within the airway smooth muscle layer correlates with age but not in cases of asthma
Source: International Congress 2016 – Translational studies in lung disease
Year: 2016
We use cookies on our website to give you the most relevant experience by remembering your preferences and repeat visits. By clicking "Accept", you consent to the use of the cookies.
Accept