scholarly journals Functional Haplotypes in the Promoter Region of Transcription FactorNrf2in Chronic Obstructive Pulmonary Disease

2010 ◽  
Vol 28 (3) ◽  
pp. 185-193 ◽  
Author(s):  
Chung-Ching Hua ◽  
Liang-Che Chang ◽  
Jo-Chi Tseng ◽  
Chien-Ming Chu ◽  
Yu-Chih Liu ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Respiratory Failure ◽  
Pulmonary Disease ◽  
Promoter Region ◽  
Gene Promoter ◽  
Chronic Obstructive Lung Disease ◽  
Disease Stage ◽  
Chronic Obstructive ◽  
Nucleotide Polymorphisms ◽  
Obstructive Pulmonary Disease

Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) protects against oxidative stress which is important in the pathogenesis of chronic obstructive pulmonary disease (COPD). Three single nucleotide polymorphisms and 1 triplet repeat polymorphism are found in the promoter region of theNrf2gene. Molecular haplotyping of theNrf2promoter region was performed using DNA obtained from the peripheral blood of 69 COPD patients. The luciferase activities ofNrf2promoter constructs containing all possible combinations of the 4 polymorphisms were determined and found to differ among the 16 haplotypes.The haplotypes isolated from the subjects were divided into 3 groups (L: low; M: medium; H: high) on the basis of luciferase activities. The proportions of subjects belonging to global initiative for chronic obstructive lung disease stage 3 or 4 decreased from the group with the LL haplotype to that with the HH haplotype. Presence of the LH or MM haplotype (hazard ratio, 3.36; 95% confidence interval, 1.16–9.69), gender (0.13; 0.02–0.67), and post-bronchodilator FEV1value of predicted (0.95; 0.91–0.99) are significant predictors of respiratory failure development.The haplotype of theNrf2gene promoter affects its activity, and is associated with the severity and the development of respiratory failure in COPD.

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.

RESPIRATORY TUBERCULOSIS AND CHRONIC OBSTRUCTIVE LUNG DISEASE - FEATURES OF THE COMORBIDE STATE

2019 ◽  
Author(s):  
Anna Viktorovna Katicheva ◽  
Nikolai Andreyevich Brazhenko ◽  
Olga Nikolaevna Brazhenko ◽  
Anna Georgievna Chuikova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Rapid Development ◽  
Chronic Obstructive Lung Disease ◽  
Chronic Obstructive ◽  
Bronchial Obstruction ◽  
Obstructive Pulmonary Disease ◽  
Diffusion Capacity ◽  
Cardiovascular Pathology ◽  
Systemic Arterial Hypertension

In modern conditions, chronic tobacco intoxication and chronic obstructive pulmonary disease are widespread and affect the health and life expectancy of patients. Among patients with tuberculosis, chronic tobacco intoxication and COPD are also widespread. Against the background of smoking and chronic obstructive pulmonary disease in patients with tuberculosis of the respiratory system, bronchial obstruction, hypoxemia, impaired capillary pulmonary blood flow, and a decrease in the diffusion capacity of the lungs are determined. A comorbid state is accompanied by the development of oxidative stress, systemic inflammation, endothelial dysfunction. Such changes in combination with dyslipidemia contribute to the development of multifocal atherogenesis, systemic arterial hypertension and the rapid development of cardiovascular pathology

scholarly journals LINC01414/LINC00824 genetic polymorphisms in association with the susceptibility of chronic obstructive pulmonary disease

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaoman Zhou ◽  
Yunjun Zhang ◽  
Yutian Zhang ◽  
Quanni Li ◽  
Mei Lin ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Genetic Polymorphisms ◽  
Chronic Obstructive ◽  
Nucleotide Polymorphisms ◽  
Obstructive Pulmonary Disease ◽  
Logistic Analysis ◽  
Copd Patients ◽  
Increased Risk ◽  
And Gender

Abstract Objective Chronic obstructive pulmonary disease (COPD) is a complicated multi-factor, multi-gene disease. Here, we aimed to assess the association of genetic polymorphisms in LINC01414/ LINC00824 and interactions with COPD susceptibility. Methods Three single nucleotide polymorphisms (SNPs) in LINC01414/LINC00824 was genotyped by Agena MassARRAY platform among 315 COPD patients and 314 controls. Logistic analysis adjusted by age and gender were applied to estimate the genetic contribution of selected SNPs to COPD susceptibility. Results LINC01414 rs699467 (OR = 0.73, 95% CI 0.56–0.94, p = 0.015) and LINC00824 rs7815944 (OR = 0.56, 95% CI 0.31–0.99, p = 0.046) might be protective factors for COPD occurrence, while LINC01414 rs298207 (OR = 2.88, 95% CI 1.31–6.31, p = 0.008) risk-allele was related to the increased risk of COPD in the whole population. Rs7815944 was associated with the reduced risk of COPD in the subjects aged > 70 years (OR = 0.29, p = 0.005). Rs6994670 (OR = 0.57, p = 0.007) contribute to a reduced COPD risk, while rs298207 (OR = 7.94, p = 0.009) was related to a higher susceptibility to COPD at age ≤ 70 years. Rs298207 (OR = 2.54, p = 0.043) and rs7815944 (OR = 0.43, p = 0.028) variants was associated COPD risk among males. Rs7815944 (OR = 0.16, p = 0.031) was related to the reduced susceptibility of COPD in former smokers. Moreover, the association between rs298207 genotype and COPD patients with dyspnea was found (OR = 0.50, p = 0.016), and rs7815944 was related to COPD patients with wheezing (OR = 0.22, p = 0.008). Conclusion Our finding provided further insights into LINC01414/LINC00824 polymorphisms at risk of COPD occurrence and accumulated evidence for the genetic susceptibility of COPD.

scholarly journals Methylation of SERPINA1 gene promoter may predict chronic obstructive pulmonary disease in patients affected by acute coronary syndrome

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
John Charles Rotondo ◽  
Giorgio Aquila ◽  
Lucia Oton-Gonzalez ◽  
Rita Selvatici ◽  
Paola Rizzo ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Acute Coronary Syndrome ◽  
Pulmonary Disease ◽  
Blood Cells ◽  
Gene Promoter ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Coronary Syndrome ◽  
Copd Patients ◽  
Potential Biomarker

Abstract Background Diagnostic biomarkers for detecting chronic obstructive pulmonary disease (COPD) in acute coronary syndrome (ACS) patients are not available. SERPINA1, coding for the most potent circulating anti-inflammatory protein in the lung, has been found to be differentially methylated in blood cells from COPD patients. This study aimed to investigate the methylation profile of SERPINA1 in blood cells from ACS patients, with (COPD+) or without COPD (COPD−). Methods Blood samples were from 115 ACS patients, including 30 COPD+ and 85 COPD− according to lung function phenotype, obtained with spirometry. DNA treated with sodium bisulfite was PCR-amplified at SERPINA1 promoter region. Methylation analysis was carried out by sequencing the PCR products. Lymphocytes count in ACS patients was recorded at hospital admission and discharge. Results SERPINA1 was hypermethylated in 24/30 (80%) COPD+ and 48/85 (56.5%) COPD− (p < 0.05). Interestingly, at hospital discharge, lymphocytes count was higher in COPD− patients carrying SERPINA1 hypermethylated (1.98 × 103 ± 0.6 cell/µl) than in COPD− carrying SERPINA1 hypomethylated (1.7 × 103 ± 0.48 cell/µl) (p < 0.05). Conclusions SERPINA1 is hypermethylated in blood cells from COPD+ patients. COPD− carrying SERPINA1 hypermethylated and high lymphocytes count may be at risk of COPD development. Therefore, SERPINA1 hypermethylation may represent a potential biomarker for predicting COPD development in ACS patients.

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