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Condition: Chronic Obstructive Pulmonary

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Total 173 results found since Jan 2013.

Mammalian target of rapamycin and p70S6K mediate thrombin-induced nuclear factor- κB activation and IL-8/CXCL8 release in human lung epithelial cells.
In conclusion, these results indicate that thrombin initiates the Akt-dependent mTOR/p70S6K signaling pathway to promote p300 phosphorylation and NF-κB activation and finally induces IL-8/CXCL8 release in human lung epithelial cells. PMID: 31863766 [PubMed - as supplied by publisher]
Source: European Journal of Pharmacology - December 17, 2019 Category: Drugs & Pharmacology Authors: Lin CH, Shih CH, Jiang CP, Wen HC, Cheng WH, Chen BC Tags: Eur J Pharmacol Source Type: research

Targeting c-Src Reverses Accelerated GPX-1 mRNA Decay in COPD Airway Epithelial Cells.
Abstract Enhanced expression of the cellular antioxidant glutathione peroxidase-1 (GPX-1) prevents cigarette smoke-induced lung inflammation and tissue destruction. COPD subjects, however, have decreased airway GPX-1 levels rendering them more susceptible to disease onset and progression. The mechanisms that down regulate GPX-1 in the airway epithelium in COPD remain unknown. To ascertain these factors, analyses were conducted using human airway epithelial cells isolated from healthy and COPD human subjects and lung tissue from control and cigarette smoke exposed A/J mice. Tyrosine phosphorylation modifies GPX-1 e...
Source: American Journal of Respiratory Cell and Molecular Biology - December 3, 2019 Category: Molecular Biology Authors: Dabo AJ, Ezegbunam W, Wyman AE, Moon J, Railwah C, Lora A, Majka SM, Geraghty P, Foronjy RF Tags: Am J Respir Cell Mol Biol Source Type: research

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

Downregulation of lysosome-associated membrane protein-2A accelerates cigarette smoke extract-induced aging and apoptosis in human bronchial epithelial cells
In this study, we evaluated the expression level of LAMP-2A in lung tissues and primary human bronchial epithelial cells (HBEC) of the normal, smoker, and COPD patients and investigated the role of LAMP-2A in cigarette smoke extract (CSE)-induced aging and death in lung epithelial cells (BEAS-2B). The protein level of LAMP-2A significantly decreased in lung homogenates from smokers and COPD patients compared with never smokers. Immunohistochemical analysis showed a significant decrease of LAMP-2A level in lung epithelial cells. Primary HBEC from smokers and COPD patients expressed a lower level of LAMP-2A than never smoker...
Source: European Respiratory Journal - November 20, 2019 Category: Respiratory Medicine Authors: Lee, K.-H., Jeong, Y., Kim, J. Y., Lee, C.-H., Yoo, C.-G. Tags: Mechanisms of lung injury and repair Source Type: research

The RNA binding protein HuR regulates the senescence-associated secretory phenotype under conditions of oxidative stress
Conclusion: Gene silencing of HuR in the presence and absence of oxidative stress results in increased expression of inflammatory mediators, MMPs and senescence markers, suggesting HuR may play a role in regulation of the SASP in COPD.
Source: European Respiratory Journal - November 20, 2019 Category: Respiratory Medicine Authors: Hassibi, S., Baker, J., Donnelly, L., Barnes, P. Tags: Airway cell biology and immunopathology Source Type: research

Lysosomal dysfunction in COPD pathogenesis
Conclusion: These findings suggest that accumulation of dysfunctional lysosome, which is attributed to reduced TRIM16-mediated lysophagy, can be associated with enhanced epithelial cell damage during COPD pathogenesis.
Source: European Respiratory Journal - November 20, 2019 Category: Respiratory Medicine Authors: Saito, N., Araya, J., Ito, A., Hosaka, Y., Ichikawa, A., Kadota, T., Nakano, T., Yoshida, M., Fujita, Y., Utsumi, H., Hashimoto, M., Wakui, H., Minagawa, S., Hara, H., Numata, T., Kaneko, Y., Kuwano, K. Tags: Airway cell biology and immunopathology Source Type: research

Chaperone-mediated autophagy modulates epithelial cell apoptosis in COPD pathogenesis
Conclusion: These findings suggest that reduced CMA activity may be involved in the mechanism for epithelial cell apoptosis by enhancing CS-induced UPR in COPD pathogenesis.
Source: European Respiratory Journal - November 20, 2019 Category: Respiratory Medicine Authors: Hosaka, Y., Araya, J., Fujita, Y., Tsubouchi, K., Minagawa, S., Hara, H., Nakano, T., Ito, A., Ichikawa, A., Saito, N., Kadota, T., Yoshida, M., Hashimoto, M., Numata, T., Kaneko, Y., Kuwano, K. Tags: Airway cell biology and immunopathology Source Type: research

Cigarette smoke decreases E-Cadherin expression downregulating FoxO3 in lung epithelial cells
Epithelial to mesenchymal transition (EMT) is implicated in lung tissue remodeling in Chronic Obstructive Pulmonary Disease (COPD). EMT is characterized by loss of epithelial junctions, including down-regulation of E-cadherin. Several signaling pathways are implicated in EMT, including TGF-β. TGF-β stimulation causes SMAD-independent activation of AKT resulting in phosphorylation and subsequent degradation of forkhead box class O3 (FoxO3). FoxO3 prevents the transcription activity of β-catenin, which controls expression of SNAIL1 and ZEB1, repressors of E-cadherin gene expression. The FoxO3 expression is red...
Source: European Respiratory Journal - November 20, 2019 Category: Respiratory Medicine Authors: Di Vincenzo, S., Sangiorgi, C., Ferraro, M., Gjomarkaj, M., Ninaber, D. K., Hiemstra, P. S., Pace, E. Tags: Airway cell biology and immunopathology Source Type: research

Allyl isothiocyanate up-regulates MRP1 expression through Notch1 signaling in human bronchial epithelial cells.
In conclusion, Notch1 signaling positively regulated MRP1 in 16HBE cells, and AITC induced MRP1 expression and function may be attributed to Notch1 signaling. These findings show that Notch1 and MRP1 might have a potential protective effect in the COPD process and become a new therapeutic target for COPD or other lung diseases. It also provides theoretical basis for the therapeutic effects of AITC. PMID: 31747319 [PubMed - as supplied by publisher]
Source: Canadian Journal of Physiology and Pharmacology - November 19, 2019 Category: Drugs & Pharmacology Authors: Li N, Guo Y, Jiang C, Zhou Y, Li C, Li Z, Wang D Tags: Can J Physiol Pharmacol Source Type: research

Cigarette Smoke Reduces Fatty Acid Catabolism, Leading to Apoptosis in Lung Endothelial Cells: Implication for Pathogenesis of COPD
Endothelial cell (EC) apoptosis contributes to cigarette smoke (CS)-induced pulmonary emphysema. Metabolism of glucose, glutamine and fatty acid is dysregulated in patients with chronic obstructive pulmonary disease (COPD). Whether CS causes metabolic dysregulation in ECs, leading to development of COPD remains elusive. We hypothesized that CS alters metabolism, resulting in apoptosis in lung ECs. To test this hypothesis, we treated primary mouse pulmonary microvascular ECs (PMVECs) with CS extract (CSE), and employed PMVECs from healthy subjects and COPD patients. We found that mitochondrial respiration was reduced in CSE...
Source: Frontiers in Pharmacology - August 28, 2019 Category: Drugs & Pharmacology Source Type: research

Inactivation of MTOR promotes autophagy-mediated epithelial injury in particulate matter-induced airway inflammation.
Abstract Particulate matter (PM) is able to induce airway epithelial injury, while the detailed mechanisms remain unclear. Here we demonstrated that PM exposure inactivated MTOR (mechanistic target of rapamycin kinase), enhanced macroautophagy/autophagy, and impaired lysosomal activity in HBE (human bronchial epithelial) cells and in mouse airway epithelium. Genetic or pharmaceutical inhibition of MTOR significantly enhanced, while inhibition of autophagy attenuated, PM-induced IL6 expression in HBE cells. Consistently, club-cell-specific deletion of Mtor aggravated, whereas loss of Atg5 in bronchial epithelium re...
Source: Autophagy - June 15, 2019 Category: Cytology Authors: Wu YF, Li ZY, Dong LL, Li WJ, Wu YP, Wang J, Chen HP, Liu HW, Li M, Jin CL, Huang HQ, Ying SM, Li W, Shen HH, Chen ZH Tags: Autophagy Source Type: research

Oligonucleotide therapy: An emerging focus area for drug delivery in chronic inflammatory respiratory diseases
Publication date: Available online 25 May 2019Source: Chemico-Biological InteractionsAuthor(s): Meenu Mehta, Deeksha, Devesh Tewari, Gaurav Gupta, Rajendra Awasthi, Harjeet Singh, Parijat Pandey, Dinesh Kumar Chellappan, Ridhima Wadhwa, Trudi Collet, Philip M. Hansbro, S Rajesh Kumar, Lakshmi Thangavelu, Poonam Negi, Kamal Dua, Saurabh SatijaAbstractOligonucleotide-based therapies are advanced novel interventions used in the management of various respiratory diseases such as asthma and Chronic Obstructive Pulmonary Disease (COPD). These agents primarily act by gene silencing or RNA interference. Better methodologies and te...
Source: Chemico Biological Interactions - May 26, 2019 Category: Biochemistry Source Type: research

Oligonucleotide therapy: An emerging focus area for drug delivery in chronic inflammatory respiratory diseases.
Abstract Oligonucleotide-based therapies are advanced novel interventions used in the management of various respiratory diseases such as asthma and Chronic Obstructive Pulmonary Disease (COPD). These agents primarily act by gene silencing or RNA interference. Better methodologies and techniques are the need of the hour that can deliver these agents to tissues and cells in a target specific manner by which their maximum potential can be reached in the management of chronic inflammatory diseases. Nanoparticles play an important role in the target-specific delivery of drugs. In addition, oligonucleotides also are ext...
Source: Chemico-Biological Interactions - May 24, 2019 Category: Molecular Biology Authors: Mehta M, Deeksha, Tewari D, Gupta G, Awasthi R, Singh H, Pandey P, Chellappan DK, Wadhwa R, Collet T, Hansbro PM, Kumar SR, Thangavelu L, Negi P, Dua K, Satija S Tags: Chem Biol Interact Source Type: research

TRPC channels mediated calcium entry is required for proliferation of human airway smooth muscle cells induced by nicotine-nAChR.
In conclusion, nicotine-induced HASMC proliferation was mediated by TRPC3-dependent calcium entry via α5-nAchR, which provided a potential target for treatment of COPD. PMID: 30550855 [PubMed - as supplied by publisher]
Source: Biochimie - December 11, 2018 Category: Biochemistry Authors: Jiang Y, Zhou Y, Peng G, Tian H, Pan D, Liu L, Yang X, Li C, Li W, Chen L, Ran P, Dai A Tags: Biochimie Source Type: research

Cigarette smoke exposure decreases CFLAR expression in bronchial epithelium, augmenting susceptibility for cell death and DAMP release
In conclusion, CS exposure decreases CFLAR expression, which might increase susceptibility to immunogenic cell death. Our study suggests that susceptibility for CS-induced airway inflammation is driven by dysregulated cell death machinery, which may be used at target for future COPD treatments.
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Pouwels, S. D., Faiz, A., Heijink, I. H., Vermeulen, C. J., Guryev, V., Van Den Berge, M., Nawijn, M. C. Tags: Mechanisms of Lung Injury and Repair Source Type: research