Chris Rider

Chris Rider
University of British Columbia - Vancouver | UBC ·  Division of Respiratory Medicine

31.78
 · 
BSc (Hons), PhD

About

66
Publications
6,873
Reads
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677
Citations
Introduction
Chris Rider currently works at the Division of Respiratory Medicine, University of British Columbia - Vancouver. Chris does research in Bioinformatics, Cell Biology and Molecular Biology to understand the effects of Air Pollution in Asthma and COPD.
Research Experience
January 2015 - January 2017
The University of Calgary
Position
  • Postdoctoral Researcher
September 2007 - present
The University of Calgary
Position
September 2005 - September 2006
AstraZeneca
Position
  • Student Intern (Sandwich Student)
Education
September 2007
The University of Calgary
Field of study
  • Respiratory Sciences
September 2003 - July 2007
The University of Warwick
Field of study
  • Biological Sciences with Industry Year (AstraZeneca)

Publications

Publications (66)
Article
Background: Air pollution's association with asthma may be due to its augmentation of allergenic effects, but the role of microRNA (miRNA) and gene expression in this synergy is unknown. Objective: We sought to determine whether exposure to allergen, exposure to diesel exhaust (DE), or coexposures modulate miRNA, gene expression, or inflammatory...
Article
By repressing inflammatory gene expression, glucocorticoids are the most effective treatment for chronic inflammatory diseases such as asthma. However, in some patients with severe disease, or who smoke or suffer from chronic obstructive pulmonary disease, glucocorticoids are poorly effective. Although many investigators focus on defects in the rep...
Article
Full-text available
In asthma and chronic obstructive pulmonary disease, activation of G(q)-protein-coupled receptors causes bronchoconstriction. In each case, the management of moderate-to-severe disease uses inhaled corticosteroid (glucocorticoid)/long-acting β(2)-adrenoceptor agonist (LABA) combination therapies, which are more efficacious than either monotherapy a...
Article
Full-text available
Binding of glucocorticoid to the glucocorticoid receptor (GR/NR3C1) may repress inflammatory gene transcription via direct, protein synthesis-independent processes (transrepression), or by activating transcription (transactivation) of multiple anti-inflammatory/repressive factors. Using human pulmonary A549 cells, we showed that 34 out of 39 IL-1β-...
Article
Full-text available
Background Glucocorticoids act on the glucocorticoid receptor (GR; NR3C1) to resolve inflammation and, as inhaled corticosteroids (ICS), are the cornerstone of treatment for asthma. However, reduced efficacy in severe disease or exacerbations indicates a need to improve ICS actions. Methods Glucocorticoid-driven transcriptomes were compared using...
Article
Air pollution exposure is estimated to contribute to approximately seven million early deaths every year worldwide and more than 3% of disability-adjusted life years lost. Air pollution has numerous harmful effects on health and contributes to the development and morbidity of cardiovascular disease, metabolic disorders, and a number of lung patholo...
Article
RATIONALE: Diesel exhaust (DE), an established model of traffic-related air pollution, contributes significantly to the global burden of asthma and may augment the effects of allergen inhalation. Newer diesel particulate-filtering technologies may increase NO2 emissions, raising questions regarding their effectiveness in reducing harm from associat...
Article
Full-text available
Background The capacity of technologies measuring DNA methylation (DNAm) is rapidly evolving, as are the options for applicable bioinformatics methods. The most commonly used DNAm microarray, the Illumina Infinium HumanMethylation450 (450K array), has recently been replaced by the Illumina Infinium HumanMethylationEPIC (EPIC array), nearly doubling...
Article
Substantial evidence indicates that cigarette smoke exposure induces resistance to glucocorticoids, the primary maintenance medication in asthma treatment. Modest evidence also suggests that air pollution may reduce the effectiveness of these critical medications. Cigarette smoke, which has clear parallels with air pollution, has been shown to indu...
Article
Full-text available
In asthma, the clinical efficacy of inhaled corticosteroids (ICSs) is enhanced by long-acting β2-adrenoceptor agonists (LABAs). ICSs, or more accurately, glucocorticoids, promote therapeutically-relevant changes in gene expression and, in primary human bronchial epithelial cells (pHBECs) and airway smooth muscle cells, this genomic effect can be en...
Article
Rationale: Air pollution may contribute to the development of allergic diseases, including asthma, by enhancing immune responses to allergen, but the effects on microRNA, messenger RNA, and inflammatory markers remain unexplored. Objectives: To determine if acute exposure to diesel exhaust and/or allergen alters expression of microRNA and genes...
Article
Diesel exhaust (DE) is a paradigm for traffic-related air pollution. Human adaptation to DE is poorly understood and currently based on oversimplified models. DE promotes allergic responses, but protein expression changes mediated by this interaction have not been systematically investigated. The aim of this study was to define the effect of inhale...
Article
ABCC4 inhibition potentiates cAMP signaling and the effect of glucocorticoids at the genomic and functional level, with implications for future asthma management.
Article
Full-text available
Sampling various compartments within the lower airways to examine human bronchial epithelial cells (HBEC) is essential for understanding numerous lung diseases. Conventional methods to identify HBEC in bronchoalveolar lavage (BAL) and wash (BW) have throughput limitations in terms of efficiency and ensuring adequate cell numbers for quantification....
Article
Purpose of review: The review aims to give an update on the literature around traffic-related air pollution (TRAP) and allergic disease in the context of global urbanization, as the most populous countries in the world face severe TRAP exposure challenges. Recent findings: As research continues to show that gene-environment interactions and epig...
Article
Rationale: Diesel exhaust (DE) exposure increases lung inflammation and promotes asthma progression. However, molecular changes after allergen-DE co-exposure are poorly elucidated. Objective: To define changes in the allergen-induced bronchial secretome enhanced by DE. Methods: Five mild asthmatics inhaled filtered air (FA) or DE (300 mg/m3) for...
Conference Paper
Introduction: Inhaled glucocorticoids (corticosteroids) act on the glucocorticoid receptor (GR, NR3C1) to control inflammation in asthma by reducing the expression of inflammatory genes. This may involve direct repression of inflammatory gene transcription by GR and induction of anti-inflammatory genes. However, GR is a transcription factor that in...
Article
Full-text available
Although inhaled glucocorticoids, or corticosteroids (ICS), are generally effective in asthma, understanding their anti-inflammatory actions in vivo remains incomplete. To characterize glucocorticoid-induced modulation of gene expression in the human airways, we performed a randomized placebo-controlled crossover study in healthy male volunteers. S...
Conference Paper
Full-text available
RATIONALE: Glucocorticoids, typically as inhaled corticosteroid (ICS), represent the main pharmacotherapeutic option for the treatment of asthma. Acting on the glucocorticoid receptor (GR, NR3C1), glucocorticoids exert anti­ inflammatory effects on target tissues by reducing the expression of numerous inflammatory genes. It is well established that...
Article
Full-text available
Acting on the glucocorticoid receptor (NR3C1), glucocorticoids are widely used to treat inflammatory diseases. However, glucocorticoid resistance often leads to suboptimal asthma control. Since glucocorticoid-induced gene expression contributes to glucocorticoid activity, the aim of this study was to use a 2×glucocorticoid response element (GRE) re...
Article
Full-text available
In asthma and chronic obstructive pulmonary disease (COPD) multiple mediators act on Gαq-linked G protein coupled receptors (GPCRs) to cause bronchoconstriction. However, acting on the airway epithelium, such mediators may also elicit inflammatory responses. In human bronchial epithelial BEAS-2B cells, regulator of G protein signalling (RGS) 2 mRNA...
Article
Exacerbations of asthma, a chronic inflammatory respiratory disease, are associated with viral upper respiratory tract infections involving human rhinovirus. Although glucocorticoids (corticosteroids) effectively control airways inflammation in many asthmatics, human rhinovirus-associated exacerbations show reduced glucocorticoid responsiveness. Us...
Article
Post hoc analysis of two phase III clinical studies found that the phosphodiesterase (PDE) 4 inhibitor, roflumilast, reduced exacerbation frequency in patients with severe chronic obstructive pulmonary disease (COPD) that were taking inhaled corticosteroids (ICS) concomitantly whereas patients not taking ICS derived no such benefit. In contrast, in...
Article
Inhaled corticosteroids (ICS) are the cornerstone of asthma pharmacotherapy and, acting via the glucocorticoid receptor (GR), reduce inflammatory gene expression. While this is often attributed to a direct inhibitory effect of the GR on inflammatory gene transcription, corticosteroids also induce the expression of anti-inflammatory genes in vitro....
Article
Due to their potent bronchodilator properties, beta(2)-adrenoceptor agonists are a mainstay of therapy in asthma. However, the effects of beta(2)-adrenoceptor agonists on inflammation are less clear. Accordingly, we have investigated the effects of beta(2)-adrenoceptor agonists on inflammatory mediator release. Transcription factor activation, and...
Article
Full-text available
In the present study, IL (interleukin)-1beta increased GM-CSF (granulocyte/macrophage colony-stimulating factor) expression from pulmonary A549 cells and primary HBE (human bronchial epithelial) cells. These responses were repressed by the glucocorticoid dexamethasone, allowing the use of A549 cells as a relevant model. IL-1beta induced GM-CSF rele...
Article
Full-text available
Prostacyclin receptor (IP-receptor) agonists display anti-inflammatory and antiviral activity in cell-based assays and in preclinical models of asthma and chronic obstructive pulmonary disease. In this study, we have extended these observations by demonstrating that IP-receptor activation also can enhance the ability of glucocorticoids to induce ge...
Article
Acting via the glucocorticoid receptor (GR), glucocorticoids exert potent anti-inflammatory effects partly by repressing inflammatory gene transcription occurring via factors such as NF-κB. In the present study, the synthetic glucocorticoid, dexamethasone, induces expression of MKP-1 (mitogen-activated protein kinase (MAPK) phosphatase-1) in human...
Article
Acting via the glucocorticoid receptor (GR), glucocorticoids exert potent anti-inflammatory effects partly by repressing inflammatory gene transcription occurring via factors such as NF-kappaB. In the present study, the synthetic glucocorticoid, dexamethasone, induces expression of MKP-1 (mitogen-activated protein kinase (MAPK) phosphatase-1) in hu...
Article
Full-text available
The mRNA-destabilizing protein tristetraprolin (TTP) negatively regulates adenine- and uridine-rich element (ARE)-containing mRNAs. In A549 pulmonary cells, TTP mRNA and both a approximately 40- and a approximately 45-kDa phosphorylated version of TTP protein were rapidly induced in response to interleukin (IL)-1beta. Analysis with IkappaBalphaDelt...

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