Abstract
INTRODUCTIONEndothelial 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.METHODSWe 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.RESULTSThe adhesion, proliferation and secretion ability of EPCs can be induced to be decreased by CSE in vitro, 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.CONCLUSIONSThe 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.
Highlights
Endothelial dysfunction appears in many smoking-related diseases, it is an important pathophysiological feature
We explored the changes of Endothelial progenitor cells (EPCs) function, the concentrations of endothelial nitric oxide synthase (eNOS) and apoptosis-inducing factor (AIF) in cell culture supernatant, Sca-1 expression, and the changes of Sca-1 promoter methylation in EPCs induced by cigarette smoke extract (CSE), and whether the dysfunction of EPCs induced by CSE is related to Sca-1 promoter methylation
The FACS test showed that most cells co-expressed PE-CD133 and FITC-CD34 (Figure 1B), while most of the cells isolated from Figure 1B co-expressed APC-Flk-1 and PerCP-Sca-1 (Figure 1C)
Summary
Endothelial dysfunction appears in many smoking-related diseases, it is 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 common in bone marrow-derived hematopoietic stem cells (HSCs), but it is 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 whether the methylation of Sca-1 is involved in EPC dysfunction. EPCs derived from bone marrow are the primary origin of endothelial cells and have a crucial effect on major vasculogenic tissues of the body including heart and lung[5]. The mechanism how cigarette smoke influences EPC function remains unknown
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