Nursing Department, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia.
Doctoral Program of Medical Science, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia.
Vasc Health Risk Manag. 2021 Mar 23;17:103-109. doi: 10.2147/VHRM.S296293. eCollection 2021.
Smoking can cause vascular damage in the form of an inflammatory reaction characterized by endothelial activation. Endothelial activation forms a pathological adaptation pattern so that it can induce the atherogenesis process. Several markers, such as E-selectin, platelet-derived micro particles (PMPs) and hematopoietic stem cell (HSC) can identify the activation of endothelial in circulating blood. Therefore, the deviation of vascular adaptation due to smoking can be detected early through the feedback mechanism between E-selectin, PMPs, and HSC.
This study aims to analyze the initial picture of the negative impact of smoking on vascular adaptation by measuring E-selectin, PMPs, and HSC in the peripheral blood circulation. Participant criteria and methods: Peripheral blood samples (5 mL) were taken from each participant, both the smoking group (n = 30) and the non-smoker group (n = 31) to obtain peripheral blood mononuclear cells (PBMNC). PBMNC was isolated using ficoll-based gradient centrifugation. The flow cytometry assay method used to measure the E-selectin, PMPs and hematopoietic stem cells.
The mean of circulating E-selectin in smokers was higher than that of non-smokers. On the other hand, the average number of PMPs and HSCs in smokers was lower than non-smokers.
Smoking increases the risk of accelerated vascular block formation, as indicated by an increase in the amount of circulating E-selectin. The increase in E-selectin in the blood vessels mediates the increased adhesion of PMPs in the vascular area so that the number of circulating PMPs in smokers decreases. The decrease in circulating PMPs decreases the signal of vascular repair, which is characterized by a decline in the number of HSCs.
吸烟会引起血管损伤，表现为以内皮细胞激活为特征的炎症反应。内皮细胞激活形成病理适应模式，从而诱导动脉粥样硬化过程。几种标志物，如 E-选择素、血小板衍生的微颗粒 (PMPs) 和造血干细胞 (HSC)，可以识别循环血液中内皮细胞的激活。因此，通过 E-选择素、PMPs 和 HSC 之间的反馈机制，可以早期检测到吸烟引起的血管适应偏差。
本研究旨在通过测量外周循环中的 E-选择素、PMPs 和 HSC，分析吸烟对血管适应的负面影响的初始图片。参与者标准和方法：从每个参与者抽取外周血样（5 毫升），包括吸烟者组（n=30）和非吸烟者组（n=31），以获得外周血单核细胞（PBMNC）。使用基于 ficoll 的梯度离心法分离 PBMNC。使用流式细胞术测定法测量 E-选择素、PMPs 和造血干细胞。
吸烟者的循环 E-选择素平均值高于不吸烟者。另一方面，吸烟者的 PMPs 和 HSCs 的平均数量低于不吸烟者。
吸烟会增加血管形成加速的风险，这表现为循环 E-选择素的增加。血管中 E-选择素的增加介导了血管区域中 PMPs 黏附的增加，从而导致吸烟者循环中 PMPs 的数量减少。循环中 PMPs 的减少降低了血管修复的信号，这表现为 HSCs 数量的下降。
