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Condition: Chronic Obstructive Pulmonary
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Total 173 results found since Jan 2013.
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
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
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
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
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
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
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
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
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
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
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
Transcriptional and Epigenetic Modulation of Human Rhinovirus-Induced CXCL10 Production by Cigarette Smoke.
Abstract
Human rhinovirus (HRV) triggers exacerbations of asthma and chronic obstructive pulmonary disease (COPD). Cigarette smoking is the primary risk factor for the development of COPD and 25% of asthmatics smoke. Smokers experience both longer and more severe colds. We previously showed that cigarette smoke extract (CSE) inhibited HRV-induced expression of a range of epithelial antiviral molecules. Here, we use CXCL10 as a model antiviral gene to examine the mechanisms by which CSE inhibits epithelial antiviral immunity. HRV-induced CXCL10 transcription depends upon activation of nuclear factor-ĸB (NF-ĸB) an...
Source: American Journal of Respiratory Cell and Molecular Biology - October 15, 2013 Category: Molecular Biology Authors: Hudy MH, Traves SL, Proud D Tags: Am J Respir Cell Mol Biol 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
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
