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Condition: Chronic Obstructive Pulmonary
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Total 173 results found since Jan 2013.
Reactive sulfur species are involved in cigarette smoke-induced cellular senescence
Conclusions: The current study suggests that the reduction in reactive sulfer species might be related to CS-induced cellular senescence.
Source: European Respiratory Journal - November 20, 2019 Category: Respiratory Medicine Authors: Yamanaka, S., Ichikawa, T., Sugiura, H., Numakura, T., Sano, H., Yamada, M., Fujino, N., Tanaka, R., Kyogoku, Y., Akaike, T., Ichinose, M. Tags: Molecular pathology and funct. genomics Source Type: research
Nicotine Induced Epithelial-Mesenchymal Transition via Wnt/β-catenin Signaling in Human Airway Epithelial Cells.
Conclusion: These results suggest that HBECs are able to undergo EMT in vitro upon nicotine stimulation via the Wnt3a/β-catenin signaling pathway.
PMID: 23204070 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - November 30, 2012 Category: Cytology Authors: Zou W, Zou Y, Zhao Z, Li B, Ran P Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research
Critical role of fractalkine (CX3CL1) in cigarette smoke-induced mononuclear cell adhesion to the arterial endothelium
Conclusions
These results suggest that CS induces functional CX3CL1 expression in arterial endothelium and leukocytes from patients with COPD show increased CX3CL1-dependent adhesiveness. Therefore, targeting the CX3CL1/CX3CR1 axis might prevent COPD-associated cardiovascular disorders.
Source: Thorax - January 15, 2013 Category: Respiratory Medicine Authors: Rius, C., Company, C., Piqueras, L., Cerda-Nicolas, J. M., Gonzalez, C., Servera, E., Ludwig, A., Morcillo, E. J., Sanz, M.-J. Tags: Health education, Smoking, Health effects of tobacco use, Tobacco use Source Type: research
Nicotine-induced epithelial-mesenchymal transition via Wnt/{beta}-catenin signaling in human airway epithelial cells
Epithelial-mesenchymal transition (EMT) has been proposed to be a mechanism in airway remodeling, which is a characteristic of chronic obstructive pulmonary disease (COPD). Studies have shown that cigarette smoke and nicotine are factors that induce Wnt/β-catenin activation, which is a pathway that has also been implicated in EMT. The main aim of this study was to test whether human bronchial epithelial cells are able to undergo EMT in vitro following nicotine stimulation via the Wnt3a/β-catenin signaling pathway. We show that nicotine activates the Wnt3a signal pathway, which leads to the translocation of β...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2013 Category: Respiratory Medicine Authors: Zou, W., Zou, Y., Zhao, Z., Li, B., Ran, P. Tags: CALL FOR PAPERS Source Type: research
Cigarette smoke enhances human rhinovirus-induced CXCL8 production via HuR-mediated mRNA stabilization in human airway epithelial cells
Background:
Human rhinovirus (HRV) triggers exacerbations of asthma and chronic obstructive pulmonary disease (COPD). Cigarette smoking is the leading risk factor for the development of COPD and 25% of asthmatics smoke. Smoking asthmatics have worse symptoms and more frequent hospitalizations compared to non-smoking asthmatics. The degree of neutrophil recruitment to the airways correlates with disease severity in COPD and during viral exacerbations of asthma. We have previously shown that HRV and cigarette smoke, in the form of cigarette smoke extract (CSE), each induce expression of the neutrophil chemoattractant and act...
Source: BioMed Central - August 30, 2013 Category: Journals (General) Authors: Magdalena H HudyDavid Proud Source Type: research
IL‐32 was involved in cigarette smoke induced pulmonary inflammation in COPD
ConclusionsThis study revealed the critical role of IL‐32 in pulmonary inflammation of COPD and smoker‐associated diseases.
Source: The Clinical Respiratory Journal - April 1, 2014 Category: Respiratory Medicine Authors: Yao Rong, Xu‐dong Xiang, Ya‐min Li, Zhen‐yu Peng, Jin‐xiu Li Tags: Original Article Source Type: research
Inflammasome activation in airway epithelial cells after multi-walled carbon nanotube exposure mediates a profibrotic response in lung fibroblasts
Conclusions:
Taken together these results demonstrate induction of a NLRP3 inflammasome dependent but TGF-beta independent pro-fibrotic response after MWCNT exposure.
Source: Particle and Fibre Toxicology - June 10, 2014 Category: Toxicology Authors: Salik HussainStacey SangtianShamika AndersonRyan SnyderJamie MarshburnAnnette RiceJames BonnerStavros Garantziotis Source Type: research
IL‐32 was involved in cigarette smoke‐induced pulmonary inflammation in COPD
ConclusionsThis study revealed the critical role of IL‐32 in pulmonary inflammation of COPD and smoker‐associated diseases.
Source: The Clinical Respiratory Journal - June 15, 2014 Category: Respiratory Medicine Authors: Yao Rong, Xu‐dong Xiang, Ya‐min Li, Zhen‐yu Peng, Jin‐xiu Li Tags: Original Article Source Type: research
Accelerating lung epithelial cell senescence in reduced CARM1 mice enhances elastase-induced emphysema
Emphysema, a key feature of chronic obstructive pulmonary disease is characterized by progressive destruction of pulmonary alveoli. Emphysema development involves alveolar senescence. CARM1, an arginine methyltransferase and transcriptional cofactor, methylating histone and non-histone proteins found crucial for regulating senescence (Wang, BMC Mol Biol 2013). We therefore, hypothesized that loss of CARM1 induces alveolar epithelial cell senescence and thus enhances the susceptibility to elastase-induced emphysema.Porcine pancreatic elastase (PPE) treated C57BL/6 (WT) or CARM1+/- mice were analyzed for lung function, histo...
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Sarker, R. S. J., Bohla, A., Amarie, O. V., Eickelberg, O., Yildirim, A. O. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research
Reduction of high mobility group nucleosome binding domain-5 protein promotes the development of emphysema
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation which is associated with an enhanced chronic inflammation and development of emphysema. However, the mechanism by which genetic alteration contributes to empyhsema development is still barely understood. In a previous study we have detected spontaneous emphysema development in HMGN5 knockout mice (Kluger E.J., et. al., JBC 2013). The HMGN5 gene encodes a nucleosomal binding protein that competes with H1 on the nucleosome and loosens the structure of chromatin. It plays an important role in transcription, replication and the repair mechanism...
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Merthan, L., Bustin, M., Eickelberg, O., Yildirim, A. O. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research
The anti-inflammatory effects of sulforaphane are not mediated by the Nrf2 pathway
Sulforaphane (SFN) is a naturally occurring compound, found in cruciferous vegetables. SFN is a potent activator of the endogenous anti-oxidant transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Due to its anti-oxidant and anti-inflammatory properties SFN has been identified as a potential treatment for a number of diseases including chronic obstructive pulmonary (COPD). We confirmed that SFN activates of the Nrf2 pathway and induces the expression of haemoxygenase (HO)-1 and NAD(P)H:Quinone Oxireductase (NQO)-1. SFN suppressed interleukin (IL)-1b-induced and IL-1b plus oxidative stress (hydrogen pero...
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Durham, A., Jazrawi, E., Rhodes, J. A., Williams, C., Kilty, I., Barnes, P., Chung, K. F., Adcock, I. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research
CARM1 Regulates Alveolar Epithelial Senescence and Elastase-induced Emphysema Susceptibility.
Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by an irreversible loss of lung function and is one of the most prevalent and severe diseases world-wide. A major feature of COPD is emphysema -the progressive loss of alveolar tissue. Coactivator-associated arginine methyltransferase-1 (CARM1) regulates histone-methylation and the transcription of genes involved in senescence, proliferation and differentiation. Complete loss of CARM1 leads to disrupted differentiation and maturation of alveolar epithelial type-II cells (ATII). We thus hypothesized that CARM1 regulates the development and progr...
Source: Am J Respir Cell Mol... - April 23, 2015 Category: Respiratory Medicine Authors: Sarker RS, John-Schuster G, Bohla A, Mutze K, Burgstaller G, Bedford MT, Königshoff M, Eickelberg O, Yildirim AÖ Tags: Am J Respir Cell Mol Biol Source Type: research
Knockdown of versican 1 blocks cigarette-induced loss of insoluble elastin in human lung fibroblasts
Publication date: 15 August 2015 Source:Respiratory Physiology & Neurobiology, Volume 215 Author(s): Lu-lu Xu , Yun-tao Lu , Jing Zhang , Lian Wu , Mervyn j Merrilees , Jie-ming Qu COPD lung is characterized by loss of alveolar elastic fibers and an increase in the chondroitin sulfate (CS) matrix proteoglycan versican V1 (V1). V1 is a known inhibitor of elastic fiber deposition and this study investigates the effects of knockdown of V1, and add-back of CS, on CCL-210 lung fibroblasts treated with cigarette smoke extract (CSE) as a model for COPD. CSE inhibited fibroblast proliferation, viability, tropoelastin syn...
Source: Respiratory Physiology and Neurobiology - June 11, 2015 Category: Respiratory Medicine Source Type: research
Increased S100A4 expression in the vasculature of human COPD lungs and murine model of smoke-induced emphysema
Conclusions:
As enhanced S100A4 expression was observed in remodeled intrapulmonary arteries of COPD patients, targeting S100A4 could serve as potential therapeutic option for prevention of vascular remodeling in COPD patients.
Source: Respiratory Research - October 20, 2015 Category: Respiratory Medicine Authors: Sebastian ReimannLudger FinkJochen WilhelmJulia HoffmannMariola BednorzMichael SeimetzIsabel DessureaultRoger TroesserBahil GhanimWalter KlepetkoWerner SeegerNorbert WeissmannGrazyna Kwapiszewska Source Type: research
Mucin 1 downregulation associates with corticoid resistance in chronic obstructive pulmonary disease and chronic rhinosinusitis with nasal polyps
Conclusion: Corticoid response that mediates GRα nuclear translocation requires MUC1-CT. The low expression of MUC1 in patients with CRSwNP or COPD may participate in corticoid resistance.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Morell, A., Milara, J., Diaz, L., Ballester, B., Peiro, T., Gonzalez, S., Banuls, P., Cortijo, J. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research
