Differences in senescence of late Endothelial Progenitor Cells in non-smokers and smokers

Kumboyono Kumboyono; Indah Nur Chomsy; Wiwit Nurwidyaningtyas; Fibe Yulinda Cesa; Cholid Tri Tjahjono; Titin Andri Wihastuti

doi:10.18332/tid/135320

Differences in senescence of late Endothelial Progenitor Cells in non-smokers and smokers

Tob Induc Dis. 2021 Jun 2:19:10. doi: 10.18332/tid/135320. eCollection 2021.

Authors

Kumboyono Kumboyono¹, Indah Nur Chomsy², Wiwit Nurwidyaningtyas², Fibe Yulinda Cesa², Cholid Tri Tjahjono³, Titin Andri Wihastuti⁴

Affiliations

¹ School of Nursing, Faculty of Medicine, University of Brawijaya, Malang, Indonesia.
² Faculty of Medicine, University of Brawijaya,Malang, Indonesia.
³ Department of Cardiology, Faculty of Medicine, University of Brawijaya, Malang, Indonesia.
⁴ Department of Basic Nursing Science, Faculty of Medicine, University of Brawijaya, Malang, Indonesia.

Abstract

Introduction: Endothelial Progenitor Cells (EPCs) are part of hematopoietic stem cells that differentiate into endothelial cells during their blood vessels' maturation process. The role of EPCs is widely known to contribute to repair of the vascular wall when endothelial dysfunction occurs. However, various risk factors for cardiovascular disease (CVD) influence EPC performance, leading to endothelial dysfunction. One EPC dysfunction is decreased amount of EPC mobilization to the injured tissue. EPC dysfunction reduces the angiogenetic function of EPCs. The vital maturation process that the EPCs must pass is the late phase. The dysfunction of late EPCs is known as senescence. This study aimed to identify and compare senescence of late EPCs, through CD62E and CD41 markers, in non-smokers and smokers as a risk factor for CVD.

Methods: EPC collection was from peripheral mononuclear cells (PBMCs) in non-smokers (n=30) and smokers (n=31). The EPCs were then marked by CD62E/CD41 and senescence β-galactosidase assay using FACS. Identification of senescence cells was based on fluorescence with DAPI.

Results: Positive percentage of late EPCs in non-smokers was not significantly different from that in smokers (p=0.014). The number of senescent late EPCs in smokers was higher than in non-smokers (p<0.0001).

Conclusions: Endothelial progenitor cells that experienced senescence in the smokers showed EPC dysfunction, which resulted in decreased cell angiogenic function. Further research is needed to explain the mechanism of re-endothelialization failure in EPC dysfunction due to smoking.

Keywords: EPC dysfunction; late EPCs; progenitor cells; senescence; smoking.