中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (46): 8693-8697.doi: 10.3969/j.issn.2095-4344.2012.46.029

• 组织构建细胞学实验 cytology experiments in tissue construction • 上一篇    下一篇

E1A激活基因阻遏子蛋白对抗人脐静脉血管内皮细胞的凋亡

闫承慧，王 娜，陶 杰，李 毅，王效增，韩雅玲   

  1. 解放军沈阳军区总医院全军心血管病研究所，辽宁省沈阳市 110840
  • 收稿日期:2012-02-24 修回日期:2012-03-19 出版日期:2012-11-11 发布日期:2013-03-16
  • 通讯作者: 韩雅玲，博士，教授，博士生导师，解放军沈阳军区总医院全军心血管病研究所心内科，110840 hanyaling@263.ne
  • 作者简介:闫承慧☆，女，1973年生，黑龙江省哈尔滨市人，汉族，2003年哈尔滨医科大学毕业，博士，副主任技师，主要从事心血管病的基础研究。 yanch1029@163.com

Cellular repressor of E1A-stimulated genes inhibits apoptosis of human umbilical vein endothelial cells

Yan Cheng-hui, Wang Na, Tao Jie, Li Yi, Wang Xiao-zeng, Han Ya-ling   

  1. Department of Cardiology, Cardiovascular Research Institute, General Hospital of Shenyang Military Area Command of Chinese PLA, Shenyang 110840, Liaoning Province, China
  • Received:2012-02-24 Revised:2012-03-19 Online:2012-11-11 Published:2013-03-16
  • Contact: Han Ya-ling, Doctor, Professor, Doctoral supervisor, Department of Cardiology, Cardiovascular Research Institute, General Hospital of Shenyang Military Area Command of Chinese PLA, Shenyang 110840, Liaoning Province, China hanyaling@263.net
  • About author:Yan Cheng-hui☆, Doctor, Associate chief technician, Department of Cardiology, Cardiovascular Research Institute, General Hospital of Shenyang Military Area Command of Chinese PLA, Shenyang 110840, Liaoning Province, China yanch1029@163.com

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被引次数

1

摘要：

背景：前期研究显示，E1A激活基因阻遏子能够通过抑制动脉平滑肌细胞的凋亡对抗动脉粥样硬化。
目的：进一步阐明E1A激活基因阻遏子在内皮细胞凋亡中的作用。
方法：通过去血清方法诱导体外培养的人脐静脉内皮细胞凋亡，然后进行TUNEL和caspase-3的活性检测。
结果与结论：伴随着E1A激活基因阻遏子的表达下降，内皮细胞的凋亡增多。功能获得和功能缺失分析显示：E1A激活基因阻遏子过表达后能够明显抑制内皮细胞的凋亡，而E1A激活基因阻遏子表达减少可以明显增加诱导内皮细胞的凋亡。进一步应用Western blot分析显示：E1A激活基因阻遏子对于内皮细胞凋亡的保护作用主要通过激活PI3K/AKT信号通路介导。提示E1A激活基因阻遏子对抗去血清诱导的内皮细胞凋亡中具有重要的作用。并且，E1A激活基因阻遏子抑制的内皮细胞凋亡可能通过PI3K/AKT信号转导通路。

关键词: E1A激活基因阻遏子, 动脉内皮, 凋亡, 动脉粥样硬化, 人脐静脉内皮细胞

Abstract:

BACKGROUND: Previous studies have demonstrated that there is a protective effect of cellular repressor of E1A-stimulated genes (CREG) against atherosclerosis through prevention of vascular smooth muscle cell apoptosis. However, the role of CREG in endothelial cells (ECs) apoptosis and its underlying signal mechanism is unknown.
OBJECTIVE: To further illustrate the effect of CREG on the apoptosis of ECs.
METHODS: The apoptosis of human umbilical vein endothelial cells (HUVECs) was induced by serum deprived culture, as well as the expression of CREG was detected by Western blot. TUNEL staining and caspase-3 activity assays were used to evaluate the apoptosis of HUVECS. Furthermore, gain- and loss-of-function analysis was used to reveal the bio-function of CREG in HUVEC apoptosis.
RESULTS AND CONCLUSION: Western blot revealed that the apoptosis of ECs was increased with the decreasing of CREG expression. Moreover, gain- and loss-of-function identified that CREG could significantly inhibit ECs apoptosis after the overexpression, whereas the decrease of CREG overexpression could obviously increased and induced. Meanwhile, Western analysis demonstrated that the protective effect of CREG on ECs apoptosis might mainly mediated by activating PI3K/AKT signaling serum starvation pathway. These results suggest that CREG plays a critical role in protecting the vascular endothelium from apoptosis, and the protective effect of CREG against ECs apoptosis may be related with the transduction of PI3K/AKT signaling pathway.

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