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Cigarette Smoke Extract Affects Methylation Status and Attenuates Sca-1 Expression of Mouse Endothelial Progenitor Cell in Vitro

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Journal Tob Induc Dis
Date 2021 Feb 5
PMID 33542680
Citations 2
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Abstract

Introduction: Endothelial dysfunction appears in many smoking-related diseases, it is also an important pathophysiological feature. Endothelial progenitor cells (EPCs) are precursors of endothelial cells and have a crucial effect on the repair and maintenance of endothelial integrity. Sca-1 is not only common in bone marrow-derived hematopoietic stem cells (HSCs), but it is also expressed in nonhematopoietic organs by tissue-resident stem and progenitor cells. The aim of this study is to investigate the impact of cigarette smoke extract (CSE) on the function of bone marrow-derived EPCs and the expression level of Sca-1 in EPCs, and also whether the methylation of Sca-1 is involved in EPC dysfunction.

Methods: We measured EPC capacities including adhesion, secretion and proliferation, the concentration of endothelial nitric oxide synthase (eNOS) and apoptosis-inducing factor (AIF) in cell culture supernatant, and also Sca-1 expression and promoter methylation in EPCs induced by CSE. Decitabine (Dec) was applied to test whether it could alter the impact caused by CSE.

Results: The adhesion, proliferation and secretion ability of EPCs can be induced to be decreased by CSE , accompanied by decreased concentrations of AIF and eNOS in cell culture supernatant and decreased Sca-1 expression in EPCs. In addition, Dec could partly attenuate the impact described above. There were no significant differences in the quantitative analysis of Sca-1 promoter methylation among different groups.

Conclusions: The decreased Sca-1 expression was related to EPC dysfunction induced by CSE. EPC dysfunction resulting from CSE may be related to methylation mechanism, but not the methylation of Sca-1 promoter.

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References
1.
Liu X, Xie C . Human endothelial progenitor cells isolated from COPD patients are dysfunctional. Mol Cell Biochem. 2011; 363(1-2):53-63. DOI: 10.1007/s11010-011-1157-y. View

2.
Mons U, Muezzinler A, Gellert C, Schottker B, Abnet C, Bobak M . Impact of smoking and smoking cessation on cardiovascular events and mortality among older adults: meta-analysis of individual participant data from prospective cohort studies of the CHANCES consortium. BMJ. 2015; 350:h1551. PMC: 4413837. DOI: 10.1136/bmj.h1551. View

3.
Chen S, Wang Z, Zhou H, He B, Hu D, Jiang H . Icariin reduces high glucose-induced endothelial progenitor cell dysfunction via inhibiting the p38/CREB pathway and activating the Akt/eNOS/NO pathway. Exp Ther Med. 2019; 18(6):4774-4780. PMC: 6861942. DOI: 10.3892/etm.2019.8132. View

4.
van Empel V, Bertrand A, Hofstra L, Crijns H, Doevendans P, De Windt L . Myocyte apoptosis in heart failure. Cardiovasc Res. 2005; 67(1):21-9. DOI: 10.1016/j.cardiores.2005.04.012. View

5.
Vahsen N, Cande C, Briere J, Benit P, Joza N, Larochette N . AIF deficiency compromises oxidative phosphorylation. EMBO J. 2004; 23(23):4679-89. PMC: 533047. DOI: 10.1038/sj.emboj.7600461. View