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Condition: Emphysema

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Total 35 results found since Jan 2013.

RNA interference targeting carbohydrate sulfotransferase 3 diminishes macrophage accumulation, inhibits MMP-9 expression and promotes lung recovery in murine pulmonary emphysema
Conclusions: CHST3 siRNA diminishes accumulation of excessive macrophages and the mediators, leading to accelerate the functional recovery from airway damage by repair of the elastin network associated with pulmonary emphysema.
Source: Respiratory Research - December 9, 2015 Category: Respiratory Medicine Authors: Yoshiro KaiKoichi TomodaHiroyuki YoneyamaMasanori YoshikawaHiroshi Kimura Source Type: research

Accelerating lung epithelial cell senescence in reduced CARM1 mice enhances elastase-induced emphysema
Emphysema, a key feature of chronic obstructive pulmonary disease is characterized by progressive destruction of pulmonary alveoli. Emphysema development involves alveolar senescence. CARM1, an arginine methyltransferase and transcriptional cofactor, methylating histone and non-histone proteins found crucial for regulating senescence (Wang, BMC Mol Biol 2013). We therefore, hypothesized that loss of CARM1 induces alveolar epithelial cell senescence and thus enhances the susceptibility to elastase-induced emphysema.Porcine pancreatic elastase (PPE) treated C57BL/6 (WT) or CARM1+/- mice were analyzed for lung function, histo...
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Sarker, R. S. J., Bohla, A., Amarie, O. V., Eickelberg, O., Yildirim, A. O. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research

Reduction of high mobility group nucleosome binding domain-5 protein promotes the development of emphysema
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation which is associated with an enhanced chronic inflammation and development of emphysema. However, the mechanism by which genetic alteration contributes to empyhsema development is still barely understood. In a previous study we have detected spontaneous emphysema development in HMGN5 knockout mice (Kluger E.J., et. al., JBC 2013). The HMGN5 gene encodes a nucleosomal binding protein that competes with H1 on the nucleosome and loosens the structure of chromatin. It plays an important role in transcription, replication and the repair mechanism...
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Merthan, L., Bustin, M., Eickelberg, O., Yildirim, A. O. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research

CARM1 Regulates Alveolar Epithelial Senescence and Elastase-induced Emphysema Susceptibility.
Abstract Chronic obstructive pulmonary disease (COPD) is characterized by an irreversible loss of lung function and is one of the most prevalent and severe diseases world-wide. A major feature of COPD is emphysema -the progressive loss of alveolar tissue. Coactivator-associated arginine methyltransferase-1 (CARM1) regulates histone-methylation and the transcription of genes involved in senescence, proliferation and differentiation. Complete loss of CARM1 leads to disrupted differentiation and maturation of alveolar epithelial type-II cells (ATII). We thus hypothesized that CARM1 regulates the development and progr...
Source: Am J Respir Cell Mol... - April 23, 2015 Category: Respiratory Medicine Authors: Sarker RS, John-Schuster G, Bohla A, Mutze K, Burgstaller G, Bedford MT, Königshoff M, Eickelberg O, Yildirim AÖ Tags: Am J Respir Cell Mol Biol Source Type: research

Increased ectodomain shedding of cell adhesion molecule 1 as a cause of type II alveolar epithelial cell apoptosis in patients with idiopathic interstitial pneumonia
Conclusions: CADM1 α-shedding appeared to be increased in all four IIP subtypes and consequently contributed to AEC apoptosis by decreasing the full-length CADM1 level. This mechanism particularly impacted f-NSIP. The molecular mechanism causing AEC apoptosis may be similar between IIP and emphysema.
Source: Respiratory Research - August 1, 2015 Category: Respiratory Medicine Authors: Azusa YoneshigeMan HagiyamaTakao InoueTakahiro MimaeTakashi KatoMorihito OkadaEisuke EnokiAkihiko Ito Source Type: research

Increased S100A4 expression in the vasculature of human COPD lungs and murine model of smoke-induced emphysema
Conclusions: As enhanced S100A4 expression was observed in remodeled intrapulmonary arteries of COPD patients, targeting S100A4 could serve as potential therapeutic option for prevention of vascular remodeling in COPD patients.
Source: Respiratory Research - October 20, 2015 Category: Respiratory Medicine Authors: Sebastian ReimannLudger FinkJochen WilhelmJulia HoffmannMariola BednorzMichael SeimetzIsabel DessureaultRoger TroesserBahil GhanimWalter KlepetkoWerner SeegerNorbert WeissmannGrazyna Kwapiszewska Source Type: research

Hydrogen Sulfide Attenuates Particulate Matter-Induced Emphysema and Airway Inflammation Through Nrf2-Dependent Manner
ConclusionHydrogen sulfide played a protect role in PM-induced mice emphysema and airway inflammation by inhibiting NLRP3 inflammasome formation and apoptosis via Nrf2-dependent pathway.
Source: Frontiers in Pharmacology - February 6, 2020 Category: Drugs & Pharmacology Source Type: research

Chromatin dynamics via HMGN5 regulates COPD susceptibility
A role for epigenetics in COPD susceptibility is emerging. We previously detected spontaneous emphysema development in HMGN5 deficient mice. HMGN5 binds to the nucleosomal core particle of chromatin, competing with histone H1, thus altering chromatin structure and function. Here we investigate the contribution of HMGN5 to the development of emphysema.COPD patient lungs were analyzed by RNAseq and immunofluorescence. B6 and Hmgn5-/- mice were treated with porcine pancreatic elastase (PPE, 40U/Kg) and analyzed on d28. siRNA knock-down of Hmgn5 in ATII cells (LA4) was followed by wound healing, apoptosis and cell proliferatio...
Source: European Respiratory Journal - October 28, 2020 Category: Respiratory Medicine Authors: Conlon, T., Dorer, J., Sarker, R., Burgstaller, G., Merthan, L., Gailus-Durner, V., Fuchs, H., Hrabe De Angelis, M., Furusawa, T., Bustin, M., Yildirim, A. O. Tags: Molecular pathology and funct. genomics Source Type: research

Involvement of < em > NEAT1 < /em > /PINK1-mediated mitophagy in chronic obstructive pulmonary disease induced by cigarette smoke or PM < sub > 2.5 < /sub >
CONCLUSIONS: Our results suggest that CS and PM2.5 exposure induce mitochondrial dysfunction, and the NEAT1/PINK1 pathway plays a critical role in the occurrence and development of COPD by regulating mitophagy.PMID:35433942 | PMC:PMC9011272 | DOI:10.21037/atm-22-542
Source: Cancer Control - April 18, 2022 Category: Cancer & Oncology Authors: Qi Lin Chao-Feng Zhang Jin-Ling Guo Jian-Lin Su Zhen-Kun Guo Huang-Yuan Li Source Type: research

Hydrogen sulfide alleviates particulate matter-induced emphysema and airway inflammation by suppressing ferroptosis
CONCLUSION: This research suggested that H2S alleviated PM-induced emphysema and airway inflammation via restoring redox balance and inhibiting ferroptosis through regulating Nrf2-PPAR-ferritinophagy signaling pathway.PMID:35490984 | DOI:10.1016/j.freeradbiomed.2022.04.014
Source: Free Radical Biology and Medicine - May 1, 2022 Category: Biology Authors: Ying Wang Sha Liao Zihan Pan Simin Jiang Jing Fan Siwang Yu Lixiang Xue Jianling Yang Shaohua Ma Tong Liu Jing Zhang Yahong Chen Source Type: research

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

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