ArticleBioMed research international2014
Dual effects of cigarette smoke extract on proliferation of endothelial progenitor cells and the protective effect of 5-aza-2'-deoxycytidine on EPCs against the damage caused by CSE.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Inhalation exposure to cigarette smoke promotes neointimal formation in mouse model of arterial injury.Archives of toxicology · 2026Article
- Review
- Cigarette smoke extract affects methylation status and attenuates Sca-1 expression of mouse endothelial progenitor cell in vitro.Tobacco induced diseases · 2021Article
- Inhibiting DNA methylation alleviates cigarette smoke extract-induced dysregulation of Bcl-2 and endothelial apoptosis.Tobacco induced diseases · 2020Article
- Cigarette Smoke Extract Changes Expression of Endothelial Nitric Oxide Synthase (eNOS) and p16(INK4a) and is Related to Endothelial Progenitor Cell Dysfunction.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- 5-Aza-2'-deoxycytidine protects against emphysema in mice via suppressing p16International journal of chronic obstructive pulmonary disease · 2017Article
- Decitabine enhances stem cell antigen-1 expression in cigarette smoke extract-induced emphysema in animal model.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Comparison between cigarette smoke-induced emphysema and cigarette smoke extract-induced emphysema.Tobacco induced diseases · 2015Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledCigarette smoke is a major public health problem associated with multitude of diseases, including pulmonary and vascular diseases. Endothelial progenitor cells (EPCs) contribute to neovascularization and play an important role in the development of these diseases. The effect of CSE on EPCs is seldom studied. The aim of the current study is to observe the effect of CSE on biological behavior of EPCs and, further, to search for potential candidate agent in protection of proliferation of EPCs against the damage caused by CSE exposure in vitro.
methodsThe proliferations of EPCs isolated from bone marrow of C57BL/6J mice were assessed by MTT after incubating the EPCs with a series of concentrations of CSE (1.0%, 2.5%, 5.0%, and 10.0%) for different times (3, 6, and 24 hours) as well as with 1.0% CSE in presence of 5-AZA-CdR for 24 hours.
resultsThe proliferations of EPCs were significantly enhanced after 3 hours of exposure to concentrations of 1.0% and 2.5% CSE but depressed when exposed to concentrations of 5.0% and 10.0% CSE. Furthermore, the 5-AZA-CdR in concentrations of 2.0 μmol/L and 5.0 μmol/L partly protected against the depression of proliferation of EPCs caused by CSE exposure.
conclusionsThe CSE showed dual effects on proliferation of EPCs isolated from mice. The 5-AZA-CdR partly protected the proliferation of EPCs against the damage caused by CSE exposure in vitro, suggesting that DNA methylation may be involved in the dysfunction of EPCs induced by CSE.
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