当前位置: X-MOL 学术Tobacco Induced Diseases › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Differences in senescence of late Endothelial Progenitor Cells in non-smokers and smokers.
Tobacco Induced Diseases ( IF 2.2 ) Pub Date : 2021-06-02 , DOI: 10.18332/tid/135320
Kumboyono Kumboyono 1 , Indah Nur Chomsy 2 , Wiwit Nurwidyaningtyas 2 , Fibe Yulinda Cesa 2 , Cholid Tri Tjahjono 3 , Titin Andri Wihastuti 4
Affiliation  

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.

中文翻译:

非吸烟者和吸烟者晚期内皮祖细胞衰老的差异。

引言 内皮祖细胞 (EPC) 是造血干细胞的一部分,在血管成熟过程中分化为内皮细胞。众所周知,当发生内皮功​​能障碍时,EPC 有助于修复血管壁。然而,心血管疾病 (CVD) 的各种危险因素影响 EPC 性能,导致内皮功能障碍。一种 EPC 功能障碍是 EPC 对受伤组织的动员量减少。EPC 功能障碍降低了 EPC 的血管生成功能。EPC 必须通过的重要成熟过程是后期。晚期 EPC 的功能障碍被称为衰老。本研究旨在通过 CD62E 和 CD41 标记物识别和比较非吸烟者和吸烟者中晚期 EPC 的衰老作为 CVD 的危险因素。方法 EPC 采集来自非吸烟者 (n=30) 和吸烟者 (n=31) 的外周单核细胞 (PBMC)。然后使用 FACS 通过 CD62E/CD41 和衰老 β-半乳糖苷酶测定标记 EPC。衰老细胞的鉴定基于 DAPI 的荧光。结果 非吸烟者晚期 EPC 阳性百分比与吸烟者无显着差异 (p=0.014)。吸烟者衰老晚期 EPC 的数量高于非吸烟者(p<0.0001)。结论吸烟者衰老的内皮祖细胞表现出EPC功能障碍,导致细胞血管生成功能下降。需要进一步的研究来解释因吸烟引起的 EPC 功能障碍中再内皮化失败的机制。然后使用 FACS 通过 CD62E/CD41 和衰老 β-半乳糖苷酶测定标记 EPC。衰老细胞的鉴定基于 DAPI 的荧光。结果 非吸烟者晚期 EPC 阳性百分比与吸烟者无显着差异 (p=0.014)。吸烟者衰老晚期 EPC 的数量高于非吸烟者(p<0.0001)。结论吸烟者衰老的内皮祖细胞表现出EPC功能障碍,导致细胞血管生成功能下降。需要进一步的研究来解释因吸烟引起的 EPC 功能障碍中再内皮化失败的机制。然后使用 FACS 通过 CD62E/CD41 和衰老 β-半乳糖苷酶测定标记 EPC。衰老细胞的鉴定基于 DAPI 的荧光。结果 非吸烟者晚期 EPC 阳性百分比与吸烟者无显着差异 (p=0.014)。吸烟者衰老晚期 EPC 的数量高于非吸烟者(p<0.0001)。结论吸烟者衰老的内皮祖细胞表现出EPC功能障碍,导致细胞血管生成功能下降。需要进一步的研究来解释因吸烟引起的 EPC 功能障碍中再内皮化失败的机制。结果 非吸烟者晚期 EPC 阳性百分比与吸烟者无显着差异 (p=0.014)。吸烟者衰老晚期 EPC 的数量高于非吸烟者(p<0.0001)。结论吸烟者衰老的内皮祖细胞表现出EPC功能障碍,导致细胞血管生成功能下降。需要进一步的研究来解释因吸烟引起的 EPC 功能障碍中再内皮化失败的机制。结果 非吸烟者晚期 EPC 阳性百分比与吸烟者无显着差异 (p=0.014)。吸烟者衰老晚期 EPC 的数量高于非吸烟者(p<0.0001)。结论吸烟者衰老的内皮祖细胞表现出EPC功能障碍,导致细胞血管生成功能下降。需要进一步的研究来解释因吸烟引起的 EPC 功能障碍中再内皮化失败的机制。
更新日期:2021-06-02
down
wechat
bug