Kotlyarov Stanislav, Kotlyarova Anna
Department of Nursing, Ryazan State Medical University, 390026 Ryazan, Russia.
Department of Pharmacology and Pharmacy, Ryazan State Medical University, 390026 Ryazan, Russia.
Membranes (Basel). 2021 Aug 31;11(9):674. doi: 10.3390/membranes11090674.
Smoking is a key modifiable risk factor for developing the chronic obstructive pulmonary disease (COPD). When smoking, many processes, including the reverse transport of cholesterol mediated by the ATP binding cassette transporter A1 (ABCA1) protein are disrupted in the lungs. Changes in the cholesterol content in the lipid rafts of plasma membranes can modulate the function of transmembrane proteins localized in them. It is believed that this mechanism participates in increasing the inflammation in COPD.
Bioinformatic analysis of datasets from Gene Expression Omnibus (GEO) was carried out. Gene expression data from datasets of alveolar macrophages and the epithelium of the respiratory tract in smokers and COPD patients compared with non-smokers were used for the analysis. To evaluate differentially expressed genes, bioinformatic analysis was performed in comparison groups using the limma package in R (v. 4.0.2), and the GEO2R and Phantasus tools (v. 1.11.0).
The conducted bioinformatic analysis showed changes in the expression of the gene associated with smoking. In the alveolar macrophages of smokers, the expression levels of were lower than in non-smokers. At the same time, in most of the airway epithelial datasets, gene expression did not show any difference between the groups of smokers and non-smokers. In addition, it was shown that the expression of in the epithelial cells of the trachea and large bronchi is higher than in small bronchi.
The conducted bioinformatic analysis showed that smoking can influence the expression of the gene, thereby modulating lipid transport processes in macrophages, which are part of the mechanisms of inflammation development.
吸烟是慢性阻塞性肺疾病（COPD）发展的一个关键可改变风险因素。吸烟时，包括由ATP结合盒转运蛋白A1（ABCA1）介导的胆固醇逆向转运在内的许多过程在肺部都会受到干扰。质膜脂筏中胆固醇含量的变化可调节定位于其中的跨膜蛋白的功能。据信这种机制参与了COPD炎症的加剧。
对来自基因表达综合数据库（GEO）的数据集进行生物信息学分析。分析使用了吸烟者和COPD患者与非吸烟者相比的肺泡巨噬细胞和呼吸道上皮数据集的基因表达数据。为了评估差异表达基因，在比较组中使用R（v. 4.0.2）中的limma包以及GEO2R和Phantasus工具（v. 1.11.0）进行生物信息学分析。
进行的生物信息学分析显示与吸烟相关基因的表达发生了变化。在吸烟者的肺泡巨噬细胞中，该基因的表达水平低于非吸烟者。同时，在大多数气道上皮数据集中，吸烟者和非吸烟者组之间的基因表达没有显示出任何差异。此外，研究表明该基因在气管和大气道上皮细胞中的表达高于小气道。
进行的生物信息学分析表明，吸烟可影响该基因的表达，从而调节巨噬细胞中的脂质转运过程，这是炎症发展机制的一部分。
