scholarly journals Identification of Proteomic Signatures in Chronic Obstructive Pulmonary Disease Emphysematous Phenotype

2021 ◽  
Vol 8 ◽  
Author(s):  
Shuang Bai ◽  
Rui Ye ◽  
Cuihong Wang ◽  
Pengbo Sun ◽  
Di Wang ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Lung Tissue ◽  
Structural Damage ◽  
Wound Repair ◽  
Underlying Mechanism ◽  
Chronic Obstructive ◽  
Tissue Samples ◽  
Obstructive Pulmonary Disease ◽  
Retinol Metabolism

Chronic obstructive pulmonary disease (COPD) is a highly heterogeneous disease. Emphysematous phenotype is the most common and critical phenotype, which is characterized by progressive lung destruction and poor prognosis. However, the underlying mechanism of this structural damage has not been completely elucidated. A total of 12 patients with COPD emphysematous phenotype (COPD-E) and nine patients with COPD non-emphysematous phenotype (COPD-NE) were enrolled to determine differences in differential abundant protein (DAP) expression between both groups. Quantitative tandem mass tag–based proteomics was performed on lung tissue samples of all patients. A total of 29 and 15 lung tissue samples from patients in COPD-E and COPD-NE groups, respectively, were used as the validation cohort to verify the proteomic analysis results using western blotting. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted for DAPs. A total of 4,343 proteins were identified, of which 25 were upregulated and 11 were downregulated in the COPD-E group. GO and KEGG analyses showed that wound repair and retinol metabolism–related pathways play an essential role in the molecular mechanism of COPD emphysematous phenotype. Three proteins, namely, KRT17, DHRS9, and FMO3, were selected for validation. While KRT17 and DHRS9 were highly expressed in the lung tissue samples of the COPD-E group, FMO3 expression was not significantly different between both groups. In conclusion, KRT17 and DHRS9 are highly expressed in the lung tissue of patients with COPD emphysematous phenotype. Therefore, these proteins might involve in wound healing and retinol metabolism in patients with emphysematous phenotype and can be used as phenotype-specific markers.

scholarly journals Xiaoqinglong Decoction Attenuates Chronic Obstructive Pulmonary Disease in Rats via Inhibition of Autophagy

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Huanan Wang ◽  
Bing Mao ◽  
Chang Chen
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Chinese Medicine ◽  
Pulmonary Disease ◽  
Lung Tissue ◽  
Structural Changes ◽  
Underlying Mechanism ◽  
Control Group ◽  
Chronic Obstructive ◽  
Pathological Changes ◽  
Obstructive Pulmonary Disease

Effective treatment for chronic obstructive pulmonary disease (COPD) and knowledge of the underlying mechanism are urgently required. Xiaoqinglong decoction (XQL) is widely used to treat COPD in Traditional Chinese Medicine, but the mechanism remains unclear. In this study, we tested the hypothesis that XQL ameliorates COPD via inhibition of autophagy in lung tissue on a rat model. Rats were divided into five groups, namely, Control group, COPD group, COPD + XQL group, COPD + Rapamycin group, and COPD + XQL + Rapamycin group. Pathological changes on cellular and molecular levels, apoptosis reflected by TdT-mediated dUTP Nick-End Labeling (TUNEL) assay, and autophagy represented by LC3II/LC3I ratio and p62 level were investigated for each group. Compared with the Control group, COPD rats exhibited structural changes and activated inflammation in the lung tissue, together with enhanced apoptosis and elevated autophagy biomarkers. XQL treatment significantly ameliorated these changes, while rapamycin augmented them. These data altogether confirmed the involvement of autophagy in the pathogenesis of COPD and suggested that XQL attenuates COPD via inhibition of autophagy.

Elevated sputum BPIFB1 levels in smokers with chronic obstructive pulmonary disease: a longitudinal study

2015 ◽  
Vol 309 (1) ◽  
pp. L17-L26 ◽  
Author(s):  
J. Gao ◽  
S. Ohlmeier ◽  
P. Nieminen ◽  
T. Toljamo ◽  
S. Tiitinen ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Lung Tissue ◽  
Induced Sputum ◽  
Chronic Obstructive ◽  
Tissue Samples ◽  
Obstructive Pulmonary Disease ◽  
Longitudinal Changes

A previous study involving a proteomic screen of induced sputum from smokers and patients with chronic obstructive pulmonary disease (COPD) demonstrated elevated levels of bactericidal/permeability-increasing fold-containing protein B1 (BPIFB1). The aim of the present study was to further evaluate the association of sputum BPIFB1 levels with smoking and longitudinal changes in lung function in smokers with COPD. Sputum BPIFB1 was characterized by two-dimensional gel electrophoresis and mass spectrometry. The expression of BPIFB1 in COPD was investigated by immunoblotting and immunohistochemistry using sputum and lung tissue samples. BPIFB1 levels were also assessed in induced sputum from nonsmokers ( n = 31), smokers ( n = 169), and patients with COPD ( n = 52) via an ELISA-based method. The longitudinal changes in lung function during the 4-year follow-up period were compared with the baseline sputum BPIFB1 levels. In lung tissue samples, BPIFB1 was localized to regions of goblet cell metaplasia. Secreted and glycosylated BPIFB1 was significantly elevated in the sputum of patients with COPD compared with that of smokers and nonsmokers. Sputum BPIFB1 levels correlated with pack-years and lung function as measured by forced expiratory volume in 1 s (FEV1) % predicted and FEV1/FVC (forced vital capacity) at baseline and after the 4-year follow-up in all participants. The changes in lung function over 4 years were significantly associated with BPIFB1 levels in current smokers with COPD. In conclusion, higher sputum concentrations of BPIFB1 were associated with changes of lung function over time, especially in current smokers with COPD. BPIFB1 may be involved in the pathogenesis of smoking-related lung diseases.

scholarly journals A Brief Review of Chronic Obstructive Pulmonary Disease

2012 ◽  
Vol 19 (6) ◽  
pp. 381-384 ◽  
Author(s):  
James C Hogg
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Chronic Obstructive Lung Disease ◽  
Disease Stage ◽  
Rapid Decline ◽  
Chronic Obstructive ◽  
Intact Specimen ◽  
Tissue Samples ◽  
Obstructive Pulmonary Disease ◽  
Computed Tomography Scanning

A recent study, based on a combination of multidetector computed tomography scanning of an intact specimen with microcomputed tomography and histological analysis of lung tissue samples, reported that the number of terminal bronchioles were reduced from approximately 44,500/lung pair in control (donor) lungs to approximately 4800/lung pair in lungs donated by individuals with very severe (Global initiative for chronic Obstructive Lung Disease stage 4) chronic obstructive pulmonary disease (COPD) treated by lung transplantation. The present short review discusses the hypothesis that a rapid rate of terminal bronchiolar destruction causes the rapid decline in lung function leading to advanced COPD. With respect to why the terminal bronchioles are targeted for destruction, the postulated mechanisms of this destruction and the possibility that new treatments are able to either prevent or reverse the underlying cause of airway obstruction in COPD are addressed.

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