DNA估计的衰老标志物与COPD相关

IF 2.7 4区 医学 Q2 GENETICS & HEREDITY Genes and Environment Pub Date : 2018-09-15 DOI:10.1183/13993003.CONGRESS-2018.PA1266
M. D. Vries, V. Guryev, T. D. Jong, J. Vonk, H. Boezen, C. V. Diemen
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引用次数: 0

摘要

据推测,异常衰老与慢性阻塞性肺病(COPD)的发病机制有关。虽然大多数研究都评估衰老和已知衰老基因的差异,但我们最近开发了一种新的方法,使用全基因组测序(WGS)在DNA水平上测量衰老标记。在这项研究中,我们的目的是测试这些衰老标志物是否与COPD有关。对36名患有慢性阻塞性肺病的非吸烟者进行了WGS(FEV1/FVC我们发现COPD受试者的端粒长度显著缩短,X染色体损失更多,线粒体DNA损失更多,而与健康对照组相比,COPD受试人的AluY逆转录转座活性更高。有趣的是,这些结果与普通人群衰老特征的观察结果一致。尽管预计T细胞比例随着年龄的增长,我们没有发现COPD受试者和健康对照组之间的这种标志物有任何差异。基于DNA水平的衰老标志物估计,我们的研究显示,与健康对照组相比,COPD受试者的衰老存在差异。我们新方法的结果证实了以前的假设,即衰老确实可能与COPD有关。
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DNA-estimated ageing markers are associated with COPD
It has been postulated that abnormal ageing is involved in the disease pathogenesis of chronic obstructive pulmonary disease (COPD). While most studies assess differences in senescence and known ageing genes, we recently developed a new approach to measure ageing markers at DNA level using whole genome sequencing (WGS). In this study, we aim to test if these ageing markers are associated with COPD. WGS was performed on 36 non-smoking subjects with COPD (FEV1/FVC We found a significant shorter telomere length, more loss of X-chromosome and more loss of mitochondrial DNA in the COPD subjects, while the AluY retrotransposition activity was higher in the COPD subjects compared to the healthy controls. Interestingly, these results are in line with the observations in ageing hallmarks in the general population. Although T-cell proportion is expected to decrease with ageing, we did not find any differences for this marker between COPD subjects and healthy controls. Based on the estimation of ageing markers at DNA level, our study shows differences in ageing in COPD subjects compared to healthy controls. Results of our new approach confirm previous hypotheses that ageing might indeed be involved in COPD.
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来源期刊
Genes and Environment
Genes and Environment Biochemistry, Genetics and Molecular Biology-Genetics
CiteScore
4.00
自引率
0.00%
发文量
24
审稿时长
27 weeks
期刊介绍: Genes and Environment is an open access, peer-reviewed journal that aims to accelerate communications among global scientists working in the field of genes and environment. The journal publishes articles across a broad range of topics including environmental mutagenesis and carcinogenesis, environmental genomics and epigenetics, molecular epidemiology, genetic toxicology and regulatory sciences. Topics published in the journal include, but are not limited to, mutagenesis and anti-mutagenesis in bacteria; genotoxicity in mammalian somatic cells; genotoxicity in germ cells; replication and repair; DNA damage; metabolic activation and inactivation; water and air pollution; ROS, NO and photoactivation; pharmaceuticals and anticancer agents; radiation; endocrine disrupters; indirect mutagenesis; threshold; new techniques for environmental mutagenesis studies; DNA methylation (enzymatic); structure activity relationship; chemoprevention of cancer; regulatory science. Genetic toxicology including risk evaluation for human health, validation studies on testing methods and subjects of guidelines for regulation of chemicals are also within its scope.
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