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BioMed Research International
Volume 2014 (2014), Article ID 640752, 9 pages
http://dx.doi.org/10.1155/2014/640752
Research Article

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

1Intensive Care Unit, The Second Xiangya Hospital, Central-South University, No. 139 Middle Renmin Road, Changsha, Hunan 410011, China
2Department of Respiratory Medicine, The Second Xiangya Hospital, Central-South University, No. 139 Middle Renmin Road, Changsha, Hunan 410011, China
3Division of Respiratory Disease, Department of Internal Medicine, The Second Xiangya Hospital, Central-South University, No. 139 Middle Renmin Road, Changsha, Hunan 410011, China
4Department of Respiratory Medicine, The Third Hospital of Changsha, No. 176 West Laodong Road, Changsha, Hunan 410015, China
5Department of Geriatric Medicine, The Second Xiangya Hospital, Central-South University, No. 139 Middle Renmin Road, Changsha, Hunan 410011, China

Received 6 November 2013; Revised 7 January 2014; Accepted 7 January 2014; Published 18 February 2014

Academic Editor: Christina Pabelick

Copyright © 2014 Zhi-Hui He et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Cigarette 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. Methods. The 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. Results. The 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. Conclusions. The 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.