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Source: European Respiratory Journal

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Total 164 results found since Jan 2013.

PDK1/RSK1-dependent C/EBP{beta} activation is involved in thrombin-induced expression of orosomucoid 1-like 3 (ORMDL3) and IL-8/CXCL8 in human lung epithelial cells
In this study, we investigated that the role of phosphoinositide-dependent kinase 1 (PDK1), ribosomal S6 kinase 1 (RSK1), and CCAAT/enhancer-binding protein β (C/EBPβ) in thrombin-induced expression of ORMDL3 and IL-8/CXCL8 in human lung epithelial cells (A549). We found that treatment of cells with thrombin caused ORMDL3 mRNA and protein expression. Thrombin-induced IL-8/CXCL8-luciferase activity or IL-8/CXCL8 release was inhibited by ORMDL3 siRNA, BX-912 (a PDK1 inhibitor), and PDK1 siRNA. Moreover, thrombin-stimulated ORMDL3 expression was attenuated by BX-912, PDK1 siRNA, RSK1 siRNA, and C/EBPβ siRNA. Th...
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Chen, B.-C., Huang, M.-F. Tags: Airway Pharmacology and Treatment Source Type: research

Transcriptional Profiling reveals Reprogramming of Airway Basal Cells in IPF
Conclusion: airway basal cells derived from distal airways are reprogrammed in IPF which results in malfunction and mislead repair processes.
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Prasse, A., Jäger, B., Carleo, A., Jonigk, D., DeLuca, D. Tags: Mechanisms of Lung Injury and Repair Source Type: research

NDP52 inhibition rescues cigarette smoke mediated impairment of autophagy in macrophages
Conclusion: Cigarette smoke increases expression of autophagic markers and impairs autophagic flux in macrophages and may be the cause of the increased NDP52 expression observed in COPD patient lungs. Knockdown of NDP52 restored the flux in CSE exposed macrophages and resulted in a reduction of autophagic makers to basal levels.
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Kono, Y., Mercado, N., Ito, K., Barnes, P., Colley, T. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research

A role for the accessory type III transforming growth factor {beta} receptor (Tgfbr3) in lung alveolarisation
Bronchopulmonary dysplasia (BPD) is a common complication of premature birth, characterised by arrested secondary septation. Molecular mechanisms of arrested secondary septation are not known. Members of the transforming growth factor (TGF)-β growth factor superfamily are accredited with key roles in lung development and BPD. We profiled lung expression of the TGF-β signaling machinery in mice in a hyperoxia-based BPD model, and detected a down-regulation Tgfbr3 expression. Using laser-capture microdissection, Tgfbr3 mRNA expression was reduced in both the lung vascular and parenchymal compartments in response to...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Pozarska, A., Niess, G., Seeger, W., Morty, R. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research

LSC Abstract - Activation of FGF9 and 18 in idiopathic pulmonary fibrosis promote survival and migration and inhibit myofibroblast differentiation of human lung fibroblasts
Key developmental lung signaling pathways are reactivated in IPF. FGF9 and FGF18 are involved in epithelial–mesenchymal interactions and are critical for lung development.We evaluated the expression of FGF9, FGF18 and FGFR in lung tissue from controls and IPF patients and assessed their effect on proliferation, survival, migration and differentiation of control and IPF human lung fibroblasts (HLF).HLF were cultured with FGF9 and FGF18. FAS-ligand induced apoptosis was assayed by measuring cleaved-PARP expression. Expression of FGFR mRNA, α-smooth muscle actin, collagen I and MMPs was analyzed with qPCR, western...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Joannes, A., Jaillet, M., Mailleux, A., Crestani, B. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research

LSC Abstract - Histone deacetylase 7 mediated metabolic remodeling: A new crosslink between pulmonary hypertension and cancer
Pulmonary arterial smooth muscle cells (PASMCs) from Pulmonary Hypertension (PH) patients and several PH animal models are characterized by suppressed mitochondria-dependent apoptosis and hyperpolarization. Similarly to lung cancer (LC) cells, PH-PASMCs have reduced glucose oxidation and increased cytoplasmic glycolysis. Protein acetylation and its enzymes such as histone deacetylases (HDACs) may play a role in the control of metabolism.We assessed the regulation of Class IIa HDACs (HDAC4, 5, 7 and 9) in human and experimental models of PH and lung cancer. By using primary culture of healthy (control-PASMCs), idiopathic de...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Gamen, E., Chelladurai, P., Grimminger, F., Savai, R., Seeger, W., Savai Pullamsetti, S. Tags: ERS Lung Science Conference 2016 Source Type: research

Targeting ASK1 in preventing airway smooth muscle growth: Implications for airway remodeling in COPD
In this study we aimed to determine the effects of ASK1 inhibition on ASM growth and pro-mitogenic signaling. We found expression of ASK1 on human lung tissue and primary human ASM cells. Pre-treatment of human ASM cells with potent and orally available ASK1 inhibitor, TCASK10 resulted in a dose-dependent reduction in mitogen (FBS, PDGF and EGF)-induced ASM growth as measured by CyQuant assay. Furthermore, the effectiveness of this pharmacological inhibition was established and replicated in gene silencing experiments where ASK1 siRNA inhibited mitogen-induced human ASM cell growth. Immunoblotting revealed that the anti-mi...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Xenaki, D., Deshpande, D., Oliver, B., Sharma, P. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research

Role of MUC1 in idiopathic pulmonary fibrosis
Conclusions: MUC1-CT is increased and activated in lung tissue of IPF patients and collaborates with TGFβ1 to induce EMT and FMT cellular transformations. Pharmacologic targeting of MUC-CT may be a promising option for the treatment of IPF.
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Ballester, B., Milara, J., Sanz, C., Gonzalez, S., Guijarro, R., Martinez, C., Cortijo, J. Tags: 1.5 Diffuse Parenchymal Lung Disease Source Type: research

MUC1-CT mediates corticosteroid responses in COPD
Conclusions: MUC1-CT mediates the anti-inflammatory properties of corticosteroids and the lack of its expression in COPD increases resistance to corticosteroids.
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Diaz, L., Milara, J., Morcillo, E., Serrano, A., Guijarro, R., Sanz, C., Cortijo, J. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research

LSC Abstract - Activation of FGF9 and 18 in idiopathic pulmonary fibrosis promote survival and migration and inhibit myofibroblast differentiation of human lung fibroblasts
Key developmental lung signaling pathways are reactivated in IPF. FGF9 and FGF18 are involved in epithelial–mesenchymal interactions and are critical for lung development.We evaluated the expression of FGF9, FGF18 and FGFR in lung tissue from controls and IPF patients and assessed their effect on proliferation, survival, migration and differentiation of control and IPF human lung fibroblasts (HLF).HLF were cultured with FGF9 and FGF18. FAS-ligand induced apoptosis was assayed by measuring cleaved-PARP expression. Expression of FGFR mRNA, α-smooth muscle actin, collagen I and MMPs was analyzed with qPCR, western...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Joannes, A., Jaillet, M., Mailleux, A., Crestani, B. Tags: ERS Lung Science Conference 2016 Source Type: research

Ribosomal protein S3 gene silencing protects against experimental allergic asthma
We reported here for the first time that RPS3 gene silencing ameliorates experimental allergic asthma, probably via interruption of NF-B activity, confirming RPS3 a novel therapeutic target for the treatment of allergic airway inflammation.
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Dong, J., Liao, W., Peh, H. Y., Chan, T. K., Tan, W. S. D., Li, L., Wong, W. S. F. Tags: 5.3 Allergy and Immunology Source Type: research

PSGR olfactory receptor: A new potential target in pulmonary arterial hypertension
Pulmonary arterial hypertension (PAH) is a rare progressive disease due to distal vascular remodeling, leading to right heart failure and death. PSGR is an olfactory receptor (OR) that has been recently detected in peripheral tissues. Moreover, PSGR overexpression is associated with pro-proliferative phenotype in prostate cancer. Since PAH vascular cells are characterized by cancer-like over-proliferation, we hypothesized that PSGR might participate in the vascular remodeling leading to PAH.Here we aimed to determine whether upregulation of PSGR is implicated in PAH pathological phenotype, and to explore PSGR as a novel th...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Courboulin, A., Quatredeniers, M., Sanz, G., Breuils-Bonnet, S., Vocelle, M., Lafond, M., Perros, F., Bonnet, S., Pajot-Augy, E., Humbert, M., Cohen-Kaminsky, S. Tags: 4.3 Pulmonary Circulation and Pulmonary Vascular Diseases Source Type: research

Systematic dissection of ORMDL3 function in vitro and in vivo
ORMDL3 on human chromosome 17q21 is a major genetic influence for childhood asthma, severe asthma and asthma exacerbations. To understand further the functional roles of ORMDL3, we established both human airway epithelial models and a recombineering-generated murine Ormdl3 knockout model. The influences of ORMDL3 on inflammatory responses in vitro and in vivo were investigated.We performed gene silencing using siRNA for two days in airway epithelium cells (A549, Beas2B and NHBE cells) after which cells were stimulated with IL1B. ORMDL3 knockdown-epithelial cells released much less IL6 and IL8 at 10 hours after stimulation ...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Zhang, Y., Dean, C., Loeser, S., Gregory, L., Lloyd, C., Moffatt, M., Cookson, W. Tags: 6.4 Genes and Environment Source Type: research

Shikonin-induced necroptosis is enhanced by the inhibition of autophagy in non-small cell lung cancer cells
In conclusion, our data indicated that shikonin treatment induced necroptosis and autophagy in NSCLC cells. In addition, inhibition of shikonin-induced autophagy enhanced necroptosis, suggesting that shikonin could be a novel therapeutic strategy against NSCLC.
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Hwang, K. E., Jeong, E. T., Kim, H. R. Tags: 11.1 Lung Cancer Source Type: research

Regulation of actin dynamics by WNT-5A: Implications for human airway smooth muscle contraction
An important feature of asthma is airway hyperresponsiveness in which the airway smooth muscle (ASM) is fundamentally involved. How asthmatic ASM differs from healthy is a current focus for research. We have shown previously that WNT-5A is increased in asthmatic ASM. Here, we tested the hypothesis that WNT-5A is a determinant of the contractile response of ASM.Using bovine smooth muscle strips, we found that pre-incubation with WNT-5A increased maximum tension by histamine. We used human ASM cells to study the underlying mechanisms. In ASM loaded with the calcium dye Fura-2, neither direct exposure to WNT-5A nor pre-incuba...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Koopmans, T., Kumawat, K., Halayko, A., Gosens, R. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research