Early Detection of Negative Smoking Impacts: Vascular Adaptation Deviation Based on Quantification of Circulated Endothelial Activation Markers
Received 8 December 2020
Accepted for publication 3 March 2021
Published 23 March 2021 Volume 2021:17 Pages 103—109
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Harry Struijker-Boudier
Kumboyono Kumboyono,1 Wiwit Nurwidyaningtyas,2 Indah Nur Chomsy,2 Titin Andri Wihastuti3
1Nursing Department, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia; 2Doctoral Program of Medical Science, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia; 3Department of Biomedicine, Faculty of Medicine, University of Brawijaya, Malang, 65145, Indonesia
Correspondence: Kumboyono Kumboyono Email [email protected]
Introduction: 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.
Purpose: 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.
Results: 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.
Conclusion: 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.
Keywords: endothelial injury, cardiovascular disease, atherosclerosis, peripheral blood mononuclear cells, smoker
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