e-learning
resources
London 2016
Tuesday, 06.09.2016
Mechanisms of disease
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
DP2/CRTh2 is expressed by ASM cells in asthma and its inhibition suppresses ASM migration
Ruth Saunders (Leicester, United Kingdom), Ruth Saunders, Michael Biddle, Adam Wright, Latifa Chachi, Amanda Sutcliffe, Rachid Berair, Christopher Brightling
Source:
International Congress 2016 – Mechanisms of disease
Session:
Mechanisms of disease
Session type:
Poster Discussion
Number:
4653
Disease area:
Airway diseases
Rating:
You must
login
to grade this presentation.
Share or cite this content
Citations should be made in the following way:
Ruth Saunders (Leicester, United Kingdom), Ruth Saunders, Michael Biddle, Adam Wright, Latifa Chachi, Amanda Sutcliffe, Rachid Berair, Christopher Brightling. DP2/CRTh2 is expressed by ASM cells in asthma and its inhibition suppresses ASM migration. Eur Respir J 2016; 48: Suppl. 60, 4653
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
Management of Severe Asthma in Pediatric Patients by an Interdisciplinary Team in a Public Hospital Setting.
Respiratory sequelae of preterm birth across the life span
Related content which might interest you:
MNK-1 inhibition reduces proliferation and CXCL10 in airway smooth muscle cells
Source: Annual Congress 2013 –Airway smooth muscle and cell biology
Year: 2013
Integrins regulate eosinophil adhesion to the airway smooth muscle cells in asthma patients
Source: International Congress 2015 – Asthma mechanisms and management
Year: 2015
Eosinophil-induced airway smooth muscle cells remodeling is attenuated by blocking of RGD-binding integrins in asthma
Source: International Congress 2016 – New findings in mucosal immunology
Year: 2016
p53 dysfunction increased mitochondrial biogenesis and bronchial smooth muscle cell proliferation in asthma
Source: International Congress 2015 – Airway remodelling: recent developments
Year: 2015
CCL2 release by airway smooth muscle is increased in asthma and promotes fibrocyte migration
Source: International Congress 2014 – Cell biology 2014
Year: 2014
FGF-2 modulates human airway smooth muscle contractile protein expression and cell stiffness
Source: Annual Congress 2013 –Airway smooth muscle and cell biology
Year: 2013
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
TGF-beta alters TRPC6 expression and calcium handling via smad2/3 in human airway smooth muscle
Source: Annual Congress 2013 –Airway smooth muscle and cell biology
Year: 2013
Airway smooth muscle contractility is increased following coculture with fibrocytes
Source: International Congress 2016 – Mechanisms of disease
Year: 2016
WNT-5A and WNT-11 as novel regulators of the contractile airway smooth muscle phenotype
Source: Annual Congress 2013 –Airway smooth muscle and cell biology
Year: 2013
A functional role for WNT-5A in driving airway myocyte proliferation
Source: Annual Congress 2013 –Growth factors at the crossroads of acute and chronic inflammation
Year: 2013
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
Regulation of actin dynamics by WNT-5A: Implications for human airway smooth muscle contraction
Source: International Congress 2016 – Studies in airway cell biology
Year: 2016
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
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
Compound A (CpdA) suppressed production of corticosteroid-resistant chemokines via GR-independent mechanisms in airway smooth muscle (ASM) cells
Source: Annual Congress 2013 –Preclinical models for the development of new drugs for respiratory diseases
Year: 2013
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
The c-jun N-terminal kinase signaling pathway regulates airway smooth muscle cell proliferation
Source: International Congress 2014 – Cell biology 2014
Year: 2014
HMGB1 is upregulated in ASM in asthma and induces ASM contraction via TLR4
Source: International Congress 2015 – Immunomodulation: basic science and clinical aspects
Year: 2015
Upregulation of airway smooth muscle (ASM) cell apoptosis may limit ASM growth during airway remodeling in experimental asthma
Source: Annual Congress 2008 - Novel mechanisms in the pathogenesis of pulmonary inflammation
Year: 2008
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