Chinese Journal of Tissue Engineering Research ›› 2012, Vol. 16 ›› Issue (46): 8693-8697.doi: 10.3969/j.issn.2095-4344.2012.46.029

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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

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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