RETRACTED ARTICLE: The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide

Perry, Mark M.; Tildy, Bernadett; Papi, Alberto; Casolari, Paolo; Caramori, Gaetano; Rempel, Karen Limbert; Halayko, Andrew J.; Adcock, Ian M.; Chung, Kian Fan

doi:10.1186/s12931-018-0788-x

Cited by 21 publications

(17 citation statements)

References 50 publications

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“…This research built further on previous findings suggesting a central role for H 2 S in the development of COPD and one of the key processes involved in COPD pathogenesis, i.e. inflammation, which appointed H 2 S as a potential therapeutic target [21,22].…”

Section: Mitochondrial Dysfunction In Lung Ageing and Diseasesupporting

confidence: 78%

Early Career Members at the ERS Lung Science Conference 2020: metabolic alterations in lung ageing and disease

Ogger

Silva

Aghapour

et al. 2020

Breathe

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Section: Mitochondrial Dysfunction In Lung Ageing and Diseasesupporting

confidence: 78%

Early Career Members at the ERS Lung Science Conference 2020: metabolic alterations in lung ageing and disease

Ogger

Silva

Aghapour

et al. 2020

Breathe

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“…H 2 S has been proposed as serving as a potent antioxidant through reactive oxygen species/reactive nitrogen species scavenging, or through post-translational modification of proteins by addition of a thiol (-SH) group onto reactive cysteine residues ( 107 ). In the lungs, H 2 S suppresses the airway smooth muscle proliferation and cytokine release, an effect that is less effective in muscle from COPD patients ( 108 ).…”

Section: Therapeutic Strategies Targeting Inflammation Oxidative Strmentioning

confidence: 99%

Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease

et al. 2020

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Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD) caused by cigarette smoke and characterized by chronic inflammation, alveolar destruction (emphysema) and bronchiolar obstruction. Ozone is a gaseous constituent of urban air pollution resulting from photochemical interaction of air pollutants such as nitrogen oxide and organic compounds. While acute exposure to ozone induces airway hyperreactivity and neutrophilic inflammation, chronic ozone exposure in mice causes activation of oxidative pathways resulting in cell death and a chronic bronchial inflammation with emphysema, mimicking cigarette smoke-induced COPD. Therefore, the chronic exposure to ozone has become a model for studying COPD. We review recent data on mechanisms of ozone induced lung disease focusing on pathways causing chronic respiratory epithelial cell injury, cell death, alveolar destruction, and tissue remodeling associated with the development of chronic inflammation and AHR. The initial oxidant insult may result from direct effects on the integrity of membranes and organelles of exposed epithelial cells in the airways causing a stress response with the release of mitochondrial reactive oxygen species (ROS), DNA, and proteases. Mitochondrial ROS and mitochondrial DNA activate NLRP3 inflammasome and the DNA sensors cGAS and STING accelerating cell death pathways including caspases with inflammation enhancing alveolar septa destruction, remodeling, and fibrosis. Inhibitors of mitochondrial ROS, NLRP3 inflammasome, DNA sensor, cell death pathways, and IL-1 represent novel therapeutic targets for chronic airways diseases underlined by oxidative stress.

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“…H 2 S ameliorates LPS-induced in ammation through the ROS/MAPK and TLR4/NF-κB signaling pathways [35]. Both endogenous and exogenous H 2 S inhibits cell proliferation and cytokine release, and inhibits ERK-1/2 and MAPKs, thus resulting in a clear anti-in ammatory response [36]. H 2 S in uences multiple biological functions of cells through inhibiting the PI3K/Akt/mTOR signaling pathway and consequently cell migration, proliferation and cell division [37].…”

Section: Signaling Pathways Associated With the H/l Ratiomentioning

confidence: 99%

Pathway-based analysis enables deeper mining of GWAS data on H/L in chickens

Wang¹,

Zhu²,

Wen³

et al. 2020

Preprint

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Background Heterophils are refers to white blood cells with phagocytosis and killing functions in the avian immune system, These cells identify and kill pathogenic microorganisms through precise regulatory mechanisms. As a simple index, the heterophil/lymphocyte ratio (H/L) in the blood reflects the immune system status of chickens. H/L is a complex trait affected by multiple genetic loci, but single nucleotide polymorphisms (SNPs) significantly associated with traits can usually explain only part of the phenotypic variation. Combining a genome-wide association study (GWAS) with pathway analysis can improve understanding of the biological pathways affecting traits. Our objective was to conduct a SNP- and pathway-based analysis to identify possible biological mechanisms involved in H/L traits. Methods GWAS for H/L was performed in 1,317 Cobb broilers to identify significant single nucleotide polymorphisms (SNPs) associated with H/L. Eight SNPs (P< 1/8,068) reached a significant level of association. The following results were obtained through a series of analyses, including pathway-based association analysis and analysis of the proportion of phenotypic variance explained by SNPs. Results On the basis of GWAS analysis results, one associated SNP (5% genome-wide significance (6.80E-6,0.05/8,068)) on GGA 1(chicken chromosome 1) and seven suggestively associated SNPs with a trend toward significance(1.24E-4, 1/8,068) on GGAs 1, 7, 13 and 19 were detected. The significant SNP on GGA 19 was in Complement C1q Binding Protein (C1QBP). The wild-type and mutant individuals showed significant differences in H/L at five loci (P< 0.05). According to the results of pathway-based analysis, nine associated pathways (P < 0.05) were identified, including small cell lung cancer, proteoglycans in cancer, sulfur relay system, pathways in cancer, gastric acid secretion and purine metabolism. By combining GWAS with pathway analysis, we found that all SNPs after QC explained 12.4% of the phenotypic variation in H/L and 53 SNPs associated with H/L explained as much as 9.7% of the phenotypic variation in H/L. Conclusions Our findings contribute to understanding of the genetic regulation of H/L and provide theoretical support.

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RETRACTED ARTICLE: The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide

Cited by 21 publications

References 50 publications

Early Career Members at the ERS Lung Science Conference 2020: metabolic alterations in lung ageing and disease

Early Career Members at the ERS Lung Science Conference 2020: metabolic alterations in lung ageing and disease

Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease

Pathway-based analysis enables deeper mining of GWAS data on H/L in chickens

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