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.
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.
复制标题
香烟烟提取物对内皮祖细胞增殖的双重影响以及5-Aza-2'-脱氧胞苷对EPC的保护作用对CSE造成的损害。
DOI：
10.1155/2014/640752
复制
发表时间：
2014
影响因子：
--
通讯作者：
Yang Y
中科院分区：
文献类型：
--
作者：
He ZH;Chen P;Chen Y;Zhu YQ;He SD;Ye JR;Liu D;Yang Y
吸烟是一个主要的公共卫生问题，与许多疾病有关，包括肺和血管疾病。内皮祖细胞（Endothelial progenitor cells，EPCs）是血管新生的重要细胞，在这些疾病的发生发展中起重要作用。CSE对EPCs的影响研究较少。本研究的目的是观察CSE对EPCs生物学行为的影响，并进一步寻找CSE对EPCs增殖的保护作用。 方法.将C57 BL/6 J小鼠骨髓分离的EPCs与一系列浓度的CSE（1.0%、2.5%、5.0%和10.0%）孵育不同时间（3、6和24 h）以及与1.0% CSE和5-AZA-CdR孵育24 h后，用MTT法检测EPCs的增殖。结果1.0%和2.5%CSE作用3 h后，EPCs增殖明显增强，而5.0%和10.0%CSE作用3 h后，EPCs增殖明显减弱。2.0 μmol/L和5.0 μmol/L的5-AZA-CdR可部分对抗CSE对EPCs增殖的抑制作用。结论. CSE对小鼠EPCs的增殖具有双重作用。5-AZA-CdR对CSE诱导的EPCs增殖具有一定的保护作用，提示DNA甲基化可能参与了CSE诱导的EPCs功能障碍。
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.
登录
查看更多内容
影响因子：
--
作者：
Kerr KM;Galler JS;Hagen JA;Laird PW;Laird-Offringa IA
通讯作者：
Laird-Offringa IA
影响因子：
56.9
作者：
Asahara, T;Murohara, T;Isner, JM
通讯作者：
Isner, JM
贝前列素钠减弱香烟烟雾提取物诱导的血管内皮细胞凋亡
影响因子：
2.8
作者：
Chen, Yan;Luo, Hong;Chen, Ping
通讯作者：
Chen, Ping
DOI：
10.1152/ajplung.90215.2008
发表时间：
2008-10-01
影响因子：
4.9
作者：
Baglole, Carolyn J.;Sime, Patricia J.;Phipps, Richard P.
通讯作者：
Phipps, Richard P.
影响因子：
5.1
作者：
Banerjee, Shuvojit;Chattopadhyay, Ranajoy;Ghosh, Arunava;Koley, Hemanta;Panda, Koustubh;Roy, Siddhartha;Chattopadhyay, Dhrubajyoti;Chatterjee, Indu B.
通讯作者：
Chatterjee, Indu B.