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Condition: Chronic Obstructive Pulmonary
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Total 173 results found since Jan 2013.
Endothelial Cell Adhesion Molecule CD146: Implications for its Role in the Pathogenesis of COPD
In this study we show that CD146 expression was significantly decreased in the lung tissue of smokers with chronic obstructive pulmonary disease (COPD) and also from rats exposed to second hand smoke (SHS). Concurrently, levels of sCD146 were increased in both the plasma and bronchoalveolar lavage fluid (BALF) of COPD patients as well as in BALF from rats exposed to SHS. Decreased or abolished CD146 protein expression in rat pulmonary micro‐ and macro‐vascular endothelial cells was found after treatment with cigarette smoke extract (CSE), proinflammatory cytokine interleukin 18 (IL‐18) or after silencing CD146 expres...
Source: The Journal of Pathology - May 3, 2013 Category: Pathology Authors: Adelheid Kratzer, Hong Wei Chu, Jonas Salys, Zakaria Moumen, Maike Leberl, Russ Bowler, Carlyne Cool, Martin Zamora, Laima Taraseviciene‐Stewart Tags: Research Article Source Type: research
Mitochondrial fragmentation in cigarette smoke induced-bronchial epithelial cell senescence.
Conclusions: CSE-induced mitochondrial fragmentation is involved in cellular senescence through the mechanism of mitochondrial ROS production. Hence, disruption of mitochondrial dynamics may be a part of the pathogenic sequence of COPD development.
PMID: 24056969 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - September 20, 2013 Category: Cytology Authors: Hara H, Araya J, Ito S, Kobayashi K, Takasaka N, Yoshii Y, Wakui H, Kojima J, Shimizu K, Numata T, Kawaishi M, Kamiya N, Odaka M, Morikawa T, Kaneko Y, Nakayama K, Kuwano K Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research
Genetic deletion of IL-17A reduces cigarette smoke-induced inflammation and alveolar type II cell apoptosis.
This study opens a new option in targeting IL-17A to modulate inflammatory response to CS and may be the bases for new therapy for COPD.
PMID: 24097560 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - October 4, 2013 Category: Cytology Authors: Chang Y, Al-Alwan L, Audusseau S, Chouiali F, Carlevaro-Fita J, Iwakura Y, Baglole CJ, Eidelman DH, Hamid Q Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research
The NF-κB family member RelB regulates microRNA miR-146a to suppress cigarette smoke-induced COX-2 protein expression in lung fibroblasts.
In this study we tested whether RelB attenuation of cigarette smoke-induced COX-2 protein is due to miR-146a. Utilizing pulmonary fibroblasts deficient in RelB expression, together with siRNA knock-down of RelB, we show the essential role of RelB in diminishing smoke-induced COX-2 protein expression despite robust activation of the canonical NF-κB pathway and subsequent induction of Cox-2 mRNA. RelB did not regulate COX-2 protein expression at the level of mRNA stability. Basal levels of miR-146a were significantly lower in Relb-deficient cells and cigarette smoke increased miR-146a expression only in Relb-expressing cell...
Source: Toxicology Letters - January 25, 2014 Category: Toxicology Authors: Zago M, de Souza AR, Hecht E, Rousseau S, Hamid Q, Eidelman DH, Baglole CJ Tags: Toxicol Lett Source Type: research
Role of PPAR{gamma} Down-regulation and Activation in COPD Cell Biology
Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory condition and a leading cause of death, with no available cure. We assessed the actions in pulmonary epithelial cells of peroxisome proliferator-activated receptor γ (PPARγ), a nuclear hormone receptor with anti-inflammatory effects, whose role in COPD is largely unknown. We found that PPARγ was down-regulated in lung tissue and epithelial cells of COPD patients, via both reduced expression and phosphorylation-mediated inhibition, whereas pro-inflammatory nuclear factor-κB (NF-κB) activity was increased. Cigarette smoking is the main risk facto...
Source: Journal of Biological Chemistry - March 6, 2014 Category: Chemistry Authors: Lakshmi, S. P., Reddy, A. T., Zhang, Y., Sciurba, F. C., Mallampalli, R. K., Duncan, S. R., Reddy, R. C. Tags: Molecular Bases of Disease Source Type: research
Real-time Imaging of ATP Release Induced by Mechanical Stretch in Human Airway Smooth Muscle Cells.
Abstract
Airway smooth muscle (ASM) cells within the airway walls are continually exposed to mechanical stimuli and exhibit various functions in response to these mechanical stresses. ATP acts as an extracellular mediator in the airway. Moreover, extracellular ATP is considered to play an important role in the pathophysiology of asthma and chronic obstructive pulmonary disease. However, it is not known whether ASM cells are cellular sources of ATP secretion in the airway. We therefore investigated whether mechanical stretch induces ATP release from ASM cells. Mechanical stretch was applied to primary human ASM cel...
Source: Am J Respir Cell Mol... - June 2, 2014 Category: Respiratory Medicine Authors: Takahara N, Ito S, Furuya K, Naruse K, Aso H, Kondo M, Sokabe M, Hasegawa Y Tags: Am J Respir Cell Mol Biol Source Type: research
Lyn Regulates Cytotoxicity in Respiratory Epithelial Cells Challenged by Cigarette Smoke Extracts.
Abstract
Cigarette smoking is associated with a series of lung diseases such as cancer, chronic obstructive pulmonary disease (COPD), and asthma. Despite the intense interest, the underlying molecular mechanism in smoking-related diseases is incompletely understood. Here, we show that Lyn is involved in cytotoxicity of respiratory epithelial cells induced by cigarette smoke extracts (CSE), an in vitro culture model for evaluating tobacco toxicity. Furthermore, exposure to CSE promotes the activation of JAK2 and STAT1, which is responsible for CSE-induced cytotoxicity. Moreover, a Lyn specific siRNA, Lyn dominant n...
Source: Current Molecular Medicine - June 2, 2014 Category: Molecular Biology Authors: Wang W, Ye Y, Li J, Li X, Zhou X, Tan D, Jin Y, Wu E, Cui Q, Wu M Tags: Curr Mol Med Source Type: research
Fibroblasts That Resist Cigarette Smoke-induced Senescence Acquire Pro-fibrotic Phenotypes.
Conclusions: Extended exposure to CSE might induce two different fibroblast phenotypes, a senescent and a pro-fibrotic phenotype. The fibroblasts that resist CSE-induced cellular senescence may contribute to the pathogenesis of IPF and could contribute to fibrotic lesions in COPD acting through a TGF-β1 mediated pathway. In contrast, the senescent cells may contribute to the pathogenesis of emphysema.
PMID: 25015975 [PubMed - as supplied by publisher]
Source: Am J Physiol Lung Ce... - July 11, 2014 Category: Respiratory Medicine Authors: Kanaji N, Basma H, Nelson AJ, Farid M, Sato T, Nakanishi M, Wang X, Michalski J, Li Y, Gunji Y, Feghali-Bostwick CA, Liu X, Rennard SI Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research
Fibroblasts that resist cigarette smoke-induced senescence acquire profibrotic phenotypes
This study assessed the effect of extended exposure to cigarette smoke extract (CSE) on tissue repair functions in lung fibroblasts. Human fetal (HFL-1) and adult lung fibroblasts were exposed to CSE for 14 days. Senescence-associated β-galactosidase (SA β-gal) expression, cell proliferation, and tissue repair functions including chemotaxis and gel contraction were assessed. HFL-1 proliferation was inhibited by CSE and nearly half of the CSE-exposed cells were SA β-gal positive after 14 days exposure, whereas 33% of adult lung fibroblasts were SA β-gal positive in response to 10% CSE exposure. The SA &b...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2014 Category: Respiratory Medicine Authors: Kanaji, N., Basma, H., Nelson, A., Farid, M., Sato, T., Nakanishi, M., Wang, X., Michalski, J., Li, Y., Gunji, Y., Feghali-Bostwick, C., Liu, X., Rennard, S. I. Tags: ARTICLES Source Type: research
Fibroblast-derived non-canonical WNT ligands contribute to attenuated alveolar epithelial repair in COPD
Conclusion: In COPD, attenuated canonical WNT signaling and disturbed alveolar epithelial cell repair may be a consequence of a shift in conditions that triggers WNT-5A secretion by fibroblasts.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Baarsma, H. A., Boczkowski, J., Yildirim, A. O., Konigshoff, M. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research
Transcription factor EB (TFEB) regulates cigarette smoke extract (CSE)-induced cellular senescence
Conclusion: These findings suggest that TFEB-mediated activation of the autophagy-lysosomal pathway plays a key regulatory role in CSE-induced cellular senescence. Thus, sufficient levels of TFEB induction may be a novel medical intervention to prevent cellular senescence in COPD pathogenesis.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Kurita, Y., Araya, J., Hara, H., Kobayashi, K., Ito, S., Takasaka, N., Wakui, H., Yoshii, Y., Minagawa, S., Kojima, J., Numata, T., Shimizu, K., Kawaishi, M., Kaneko, Y., Nakayama, K., Kuwano, K. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research
Chronic treatment of {beta}-blocker inhibited mucus hypersecretion and MUC5AC expression exposed to cigarette smoking through {beta}-arrestin2-ERK1/2 pathway
CONCLUSION β2-AR-β-arrestin2–ERK1/2 signaling is required for cigarette smoke-induced MUC5AC expression. Chronic treatment of β-blocker improved airway mucus hypersecretion resulting from smokingwithout increased the contractile response. Those data may contribute to the optimization of β2-AR target therapy in COPD.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: He, B., Zhou, Y., Guo, Y., Xu, M., Zhang, Y. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research
Integrative Analysis of DNA Methylation and Gene Expression Data Identifies EPAS1 as a Key Regulator of COPD
by Seungyeul Yoo, Sachiko Takikawa, Patrick Geraghty, Carmen Argmann, Joshua Campbell, Luan Lin, Tao Huang, Zhidong Tu, Robert Feronjy, Avrum Spira, Eric E. Schadt, Charles A. Powell, Jun Zhu
Chronic Obstructive Pulmonary Disease (COPD) is a complex disease. Genetic, epigenetic, and environmental factors are known to contribute to COPD risk and disease progression. Therefore we developed a systematic approach to identify key regulators of COPD that integrates genome-wide DNA methylation, gene expression, and phenotype data in lung tissue from COPD and control samples. Our integrative analysis identified 126 key regulators...
Source: PLoS Genetics - January 8, 2015 Category: Genetics & Stem Cells Authors: Seungyeul Yoo et al. Source Type: research
Caveolin-1 aggravates cigarette smoke extract-induced MUC5AC secretion in human airway epithelial cells.
In this study, we aimed to determine whether caveolin-1 modulates mucin hyperproduction induced by cigarette smoke. Our results revealed that cigarette smoke extract (CSE) significantly increased MUC5AC production, as well as the levels of phosphorylated EGFR (p-EGFR) and phosphorylated Akt (p-Akt) in human bronchial epithelial cells (16HBE cells), as shown by ELISA, RT-PCR and western blot analysis. These effects were prevented by treatment with EGFR inhibitor (AG1478) and phosphatidylinostol-3-kinase (PI3K) inhibitor (LY294002). We also found that the overexpression of caveolin-1 enhanced the expression of MUC5AC, p-EGFR...
Source: International Journal of Molecular Medicine - March 11, 2015 Category: Molecular Biology Authors: Yu Q, Chen X, Fang X, Chen Q, Hu C Tags: Int J Mol Med Source Type: research
Decreased expression of the NF-κB family member RelB in lung fibroblasts from Smokers with and without COPD potentiates cigarette smoke-induced COX-2 expression
Conclusions:
Our data indicate that RelB attenuates COX-2 expression in lung structural cells, such that loss of pulmonary RelB may be an important determinant in the aberrant, heightened inflammation associated with COPD pathogenesis.
Source: Respiratory Research - May 6, 2015 Category: Respiratory Medicine Authors: Jared SheridanMichela ZagoParameswaran NairPei LiJean BourbeauWan TanQutayba HamidDavid EidelmanAndrea BenedettiCarolyn Baglole Source Type: research
