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Source: European Respiratory Journal

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Total 164 results found since Jan 2013.

MKP-5 inhibition blunts fibrotic responses in-vitro and in-vivo through negative regulation of TGFB1-induced smad3-signalling
Conclusion: We conclude that intact MKP5 is required for induction of changes in lung fibroblasts in-vitro and during bleomycin-induced lung fibrosis in-vivo. Our results couple MKP5 activity with TGFB1 signaling machinery identifying MKP5 inhibition as a promising therapeutic strategy for experimental and human lung fibrosis.
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Tzouvelekis, A., Xylourgidis, N., Min, K., Karampitsakos, T., Ninou, I., Barbayianni, I., Bennett, A., Aidinis, V., Kaminski, N. Tags: Mechanisms of Lung Injury and Repair Source Type: research

Involvement of GPx4-regulated lipid peroxidation in IPF pathogenesis.
Conclusion: These findings suggest that GPx4 expression levels were reduced in IPF and GPx4-regulated lipid peroxidation can be involved in IPF pathogenesis via modulating TGF-b-induced myofibroblast differentiation.
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Tsubouchi, K., Araya, J., Minagawa, S., Hara, H., Hosaka, Y., Ichikawa, A., Saito, N., Yoshida, M., Ishikawa, T., Numata, T., Kaneko, Y., Nakayama, K., Kuwano, K. Tags: Mechanisms of Lung Injury and Repair Source Type: research

TRAP1 downregulation could overcome gefitinib resistance in NSCLC via EMT reversal
In conclusions, these results suggested that TRAP1 downregulation could overcome gefitinib resistance in NSCLC via EMT reversal in tumor microenvironment.
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Hwang, K. E., Oh, S. J., Jeong, E. T., Kim, H. R. Tags: Lung Cancer Source Type: research

Inhibitory effects of mitochondrial TRAP1 on gefitinib-resistancein non-small lung cancer cells
This study was designed to investigate overcoming gefitinib resistance in NSCLC through a mechanism-based approach using gamitrinib variant containing triphenylphosphonium (G-TPP), TRAP1 inhibitor.We developed an in vitro model of acquired resistance to gefitinib. The effects of G-TPP on apoptosis and ROS-dependent mitochondrial dysfunction in HCC827GR cells were examined by annexin V binding assay, MitoSoX, and immunoblot analysis. and we tested the effects of pretreated with NAC or DPI, free radical scavenger. In addition, TRAP1 and antioxidant MnSOD were respectively knocked down or overexpressed to determine its role i...
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Hwang, K. E., Oh, S. J., Jeong, E. T., Kim, H. R. Tags: Lung Cancer Source Type: research

Club Cell Protein-16 modifies airway inflammation in asthma and is associated with significant clinical asthma outcomes
Conclusion: Lack of CC16 results in enhanced T2 inflammatory responses in both human primary cell culture and a mouse model. CC16 mRNA levels inversely correlated with MUC5AC which was supported by the CC16 knockdown experiments, and significantly associated with clinically relevant asthma outcomes.
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Kraft, M., Ledford, J., Gozdz, J., Li, X., Francisco, D., Manne, A., Guerra, S., Martinez, F., Kaminski, N., Wenzel, S., Meyers, D., Bleecker, E. Tags: Clinical Problems Source Type: research

LSC - 2017 - Re-education of tumor-associated macrophages by modulating histone deacetylases in lung cancer
Conclusions: Suppression of HDAC2 switches M2-like TAMs into M1-like phenotype and regulates tumor cell functions. Modulation of HDAC2 may provide a novel strategy for TAMs repolarization and cancer therapy.
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Zheng, X. Tags: Lung Cancer Source Type: research

LSC - 2017 - The role of the epigenetic regulator HMGN5 in COPD resulting from chronic lung injury
COPD, characterized by chronic bronchitis, small airway remodeling and emphysema, is one of the leading causes of chronic morbidity and mortality worldwide. Chronic lung injury, commonly caused by cigarette smoking (CS), is a major factor in its development. A role for epigenetics in this underlying pathology is emerging. We previously detected spontaneous emphysema in HMGN5-/-mice. HMGN5 binds to the nucleosomal core particle of chromatin, competing with histone H1, altering chromatin structure and affecting cellular transcription, differentiation and repair. Indeed, increased expression of HMGN5 has been observed in lung...
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Gunes, G., Conlon, T., Sarker, R., Burgstaller, G., Gailus-Durner, V., Fuchs, H., Hrabe de Angelis, M., Furusawa, T., Bustin, M., Eickelberg, O., Önder Yildirim, A., Dorer, J. Tags: Molecular Pathology and Functional Genomics Source Type: research

Decreased expression of FENDRR, a lung mesenchymal long non-coding RNA, regulates fibroblast phenotypes in IPF through NOX4
Conclusions: Decreased FENDRR expression may confer the altered phenotypes such as myofibroblastic differentiation and cellular senescence in IPF fibroblasts. Imbalanced redox balance, possibly through increased NOX4 levels may be involved in the mechanism.
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Sakamoto, K., Xylourgidis, N., Omote, N., Adams, T., Yu, G., Ahangari, F., Herazo-Maya, J., Kaminski, N., Homer, R. Tags: Molecular Pathology and Functional Genomics Source Type: research

DJ-1 and its anti-oxidative stress response regulates the expression of sirtuin-1 in COPD epithelial cells
Conclusions: DJ-1 binds and regulates the expression of SIRT1 in epithelial cells. As both DJ-1 and SIRT1 were down-regulated in COPD, the association of these molecules may be a mechanism of impaired anti-ageing and defence against oxidative stress in COPD.
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Koga, T., Vuppusetty, C., Ito, K., Barnes, P. J., Baker, J. R. Tags: Airway Cell Biology and Immunopathology Source Type: research

Late Breaking Abstract - Roles of setd8 in maintaining genomic integrity and tumourgenesis
Conclusions: SETD8 is vital to preserve genomic integrity by the control of origin firing. Its key role in cell proliferation presents a new target for cancer therapy. Combined inhibition of SETD8 and WEE1 may also be a new strategy in clinical treatment.
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: li, m., Liao, H., Zhu, C., Wu, Y., Wu, Y., Chen, Z., Ying, S., Shen, H., Li, W., Geng, X. Tags: Lung Cancer Source Type: research

Regulatory mechanims of ER-{beta} of OPN-Integrin interaction in the migration of human lung cancer cells
Conclusions: E2-ER-βpromotes the migration of lung cancer cells through regulating the interaction between OPN and Integrin. The E2-ER-β-OPN-Integrin axis may be a potential target in the prevention and treatment of lung cancer.
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Dong, N., Chen, C. Tags: Lung Cancer Source Type: research

RNA-binding protein HuR inhibits the expression of sirtuin-1 in patients with COPD
Conclusions: Our results indicate that HuR expression is inhibited by oxidative stress, suggesting a potential mechanism by which SIRT1 is reduced in COPD patients, leading to the accelerated ageing phenotype.
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Baker, J. R., Vuppusetty, C., Ito, K., Barnes, P., Yasuo, K. Tags: Airway Cell Biology and Immunopathology Source Type: research

TGF-{beta} participates in epithelial-mesenchymal transition in pleural fibrosis via targeting S100A4
In this study, we detected the expression of S100A4, EMT- and ECM-related markers in Met-5A cells treated with TGF-β or TGF-β inhibitor by real-time PCR, western blot and ELISA. In order to explore the role of S100A4, we used siRNA to knock down the expression of S100A4 in cell model. We found the expression of epithelial cell marker was decreased and the mesenchymal cell marker increased with ECM deposition and S100A4 up-regulation after treatment with TGF-β. Moreover, the changes of EMT-related event were restricted when the expression of S100A4 was knocked down. Conversely, S100A4 can partially rescue the...
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Sun, Z., Ning, Q., Li, F., Wang, L., Li, H., Yao, Y., Hu, T. Tags: Pleural and Mediastinal Malignancies Source Type: research

Late Breaking Abstract - ND-L02-s0201 treatment leads to efficacy in preclinical IPF models
Conclusions: Given the significant unmet medical need and our results, the safety and efficacy of ND-L02-s0201 warrants evaluation in IPF clinical trials.
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Zabludoff, S., Liu, Y., Liu, J., Zhang, J., Xia, F., Quimbo, A., Yao, J., Clamme, J.-P., Pham Siegmund, A., Maruyama, K., Ying, W. Tags: Diffuse Parenchymal Lung Disease Source Type: research

Gene regulatory roles for lysyl oxidases in the context of BPD
We report, for the first time a transcriptome-wide analysis of gene regulation by lysyl oxidases. In the context of primary mouse lung fibroblasts, siRNA knockdown of Lox, Loxl1, and Loxl2 deregulated the expression of 134, 3,761 and 3,554 genes, respectively. Identified lysyl oxidases target-genes relevant to lung development and BPD included Mmp3, Mmp9, Eln, Rarres1, Gdf10, Ifnb1, Cxcl2, and Cxcl9. The expression of target-genes in vivo correlated with the lysyl oxidases expression in a mouse model of BPD. Moreover, using BAPN, we demonstrated that the transcriptional regulation by lysyl oxidases was independent of catal...
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Mizikova, I., Palumbo, F., Morty, R., Seeger, W. Tags: Lung and Airway Developmental Biology Source Type: research