Inflammation, chronic obstructive pulmonary disease and aging

Provinciali, Mauro; Cardelli, Maurizio; Marchegiani, Francesca

doi:10.1097/01.mcp.0000410742.90463.1f

Cited by 52 publications

(43 citation statements)

References 61 publications

(87 reference statements)

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“…The observation that telomere length in circulating leukocytes of COPD patients are shorter than those of controls, is likely due to the increased systemic oxidative stress, in line with what has been observed in other chronic inflammatory disorders associated to telomere shortening [24,26–29]. …”

Section: Oxidative Dna Damagesupporting

confidence: 77%

DNA Damage Due to Oxidative Stress in Chronic Obstructive Pulmonary Disease (COPD)

Neofytou

Tzortzaki

Chatziantoniou

et al. 2012

IJMS

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According to the American Thorasic Society (ATS)/European Respiratory Society (ERS) Statement, chronic obstructive pulmonary disease (COPD) is defined as a preventable and treatable disease with a strong genetic component, characterized by airflow limitation that is not fully reversible, but is usually progressive and associated with an enhanced inflammatory response of the lung to noxious particles or gases. The main features of COPD are chronic inflammation of the airways and progressive destruction of lung parenchyma and alveolar structure. The pathogenesis of COPD is complex due to the interactions of several mechanisms, such as inflammation, proteolytic/antiproteolytic imbalance, oxidative stress, DNA damage, apoptosis, enhanced senescence of the structural cells and defective repair processes. This review focuses on the effects of oxidative DNA damage and the consequent immune responses in COPD. In susceptible individuals, cigarette smoke injures the airway epithelium generating the release of endogenous intracellular molecules or danger-associated molecular patterns from stressed or dying cells. These signals are captured by antigen presenting cells and are transferred to the lymphoid tissue, generating an adaptive immune response and enhancing chronic inflammation.

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Section: Oxidative Dna Damagesupporting

confidence: 77%

DNA Damage Due to Oxidative Stress in Chronic Obstructive Pulmonary Disease (COPD)

Neofytou

Tzortzaki

Chatziantoniou

et al. 2012

IJMS

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“…Accelerated aging, which can occur independently of and earlier than chronological aging, is a collection of molecular and cellular alterations that has been implicated in several diseases (for example, emphysema, Parkinson’s disease, diabetes, coronary artery disease). Some of these processes include: (1) cellular senescence, telomere attrition, persistent DNA damage response, and cell cycle arrest, leading to decreased cell proliferation and stimulation of T-helper type 1-associated inflammation; (2) mitochondrial dysfunction leading to increased production of free radicals and oxidative stress; and (3) decreased removal of damaged proteins leading to further cellular senescence and increased tissue damage [49-52]. Chronic exposure to cigarette smoke leads to chronic oxidative stress that has been implicated in turning on these aging processes prematurely.…”

Section: Discussionmentioning

confidence: 99%

miR-638 regulates gene expression networks associated with emphysematous lung destruction

et al. 2013

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BackgroundChronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by varying degrees of emphysematous lung destruction and small airway disease, each with distinct effects on clinical outcomes. There is little known about how microRNAs contribute specifically to the emphysema phenotype. We examined how genome-wide microRNA expression is altered with regional emphysema severity and how these microRNAs regulate disease-associated gene expression networks.MethodsWe profiled microRNAs in different regions of the lung with varying degrees of emphysema from 6 smokers with COPD and 2 controls (8 regions × 8 lungs = 64 samples). Regional emphysema severity was quantified by mean linear intercept. Whole genome microRNA and gene expression data were integrated in the same samples to build co-expression networks. Candidate microRNAs were perturbed in human lung fibroblasts in order to validate these networks.ResultsThe expression levels of 63 microRNAs (P < 0.05) were altered with regional emphysema. A subset, including miR-638, miR-30c, and miR-181d, had expression levels that were associated with those of their predicted mRNA targets. Genes correlated with these microRNAs were enriched in pathways associated with emphysema pathophysiology (for example, oxidative stress and accelerated aging). Inhibition of miR-638 expression in lung fibroblasts led to modulation of these same emphysema-related pathways. Gene targets of miR-638 in these pathways were amongst those negatively correlated with miR-638 expression in emphysema.ConclusionsOur findings demonstrate that microRNAs are altered with regional emphysema severity and modulate disease-associated gene expression networks. Furthermore, miR-638 may regulate gene expression pathways related to the oxidative stress response and aging in emphysematous lung tissue and lung fibroblasts.

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“…Recent evidence suggests that inflammatory processes, such as an increase in cytokines, chemokines, and acute-phase reactant proteins in response to environmental stimuli, particularly smoking, may play important roles in the development of COPD (Kardos and Keenan, 2006). Therefore, numerous genes involved in inflammatory processes have been considered to be associated with COPD (Provinciali et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Association of Polymorphisms of the Receptor for Advanced Glycation End Products Gene with COPD in the Chinese Population

Cheng²,

Ma³

et al. 2014

DNA and Cell Biology

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The receptor for advanced glycation end products (RAGE) is a cell surface molecule of the immunoglobulin superfamily that binds diverse endogenous ligands involved in the development of chronic diseases and inflammatory damage. A growing body of evidence has suggested that RAGE is involved in the development and progression of chronic obstructive pulmonary disease (COPD). The present study investigated the existence of an association among three polymorphisms (-374T/A, -429T/C, and G82S) of the RAGE gene with the risk of COPD in the Chinese population. The RAGE genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism in 216 patients with COPD and 239 age-matched healthy individuals. Our study demonstrated that the frequencies of the GS genotype and the S allele in the G82S mutation were significantly higher in COPD patients than in controls (odds ratios [OR]=1.70, 95% confidence interval [CI]: 1.15-2.50, p=0.0098 and OR=1.42, 95% CI: 1.06-1.91, p=0.023, respectively). Further stratification analysis by smoking status revealed that the presence of the GS genotype conferred a higher risk of developing COPD in current smokers (p=0.044). In contrast, mutations at -374T/A and -429T/C did not demonstrate any association with COPD, even after taking into account the patients' smoking history. Our study provides preliminary evidence that the G82S polymorphism in the RAGE gene is associated with an increased risk of COPD and that the GS genotype of the G82S variant is a risk factor for COPD in the Chinese population.

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Inflammation, chronic obstructive pulmonary disease and aging

Cited by 52 publications

References 61 publications

DNA Damage Due to Oxidative Stress in Chronic Obstructive Pulmonary Disease (COPD)

DNA Damage Due to Oxidative Stress in Chronic Obstructive Pulmonary Disease (COPD)

miR-638 regulates gene expression networks associated with emphysematous lung destruction

Association of Polymorphisms of the Receptor for Advanced Glycation End Products Gene with COPD in the Chinese Population

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