Reduction of connexin43 in human endothelial progenitor cells impairs the angiogenic potential

被引:51
作者
Wang, Hsueh-Hsiao [1 ,2 ]
Su, Cheng-Huang [2 ,3 ,4 ]
Wu, Yih-Jer [1 ,3 ]
Li, Jiun-Yi [5 ]
Tseng, Ya-Ming [1 ]
Lin, Yi-Chun [2 ]
Hsieh, Chin-Ling [2 ]
Tsai, Cheng-Ho [1 ,3 ]
Yeh, Hung-I [1 ,3 ]
机构
[1] Mackay Med Coll, Dept Med, New Taipei City 252, Taiwan
[2] Mackay Mem Hosp, Dept Med Res, Taipei, Taiwan
[3] Mackay Mem Hosp, Dept Internal Med, Taipei, Taiwan
[4] Mackay Med Nursing & Management Coll, Taipei, Taiwan
[5] Mackay Mem Hosp, Dept Surg, Taipei, Taiwan
关键词
Angiogenesis; Connexin43; Connexins; Endothelial progenitor cell; ARSENIC TRIOXIDE; GAP-JUNCTIONS; GROWTH-FACTOR; EXPRESSION;
D O I
10.1007/s10456-013-9335-z
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Our previous work showed that arsenic trioxide down-regulated Cx43 and attenuated the angiogenic potential of human late endothelial progenitor cells (EPC). However, the relation between Cx43 and angiogenic activity of the EPC remained unclear. In the study, human late EPC were treated with siRNA specific to Cx43 (Cx43siRNA). The expression profiles as well as activity of the treated cells were examined. In parallel, the angiogenic potential of human EPC treated with Cx43siRNA was evaluated using murine hind limb ischemic model. The results showed that, in the EPC treated with Cx43siRNA, the activity of migration, proliferation, and angiogenic potential were attenuated, accompanied by reduction in vascular endothelial growth factor (VEGF) expression. In hind limb ischemia mice, EPC treated with Cx43siRNA lost the therapeutic angiogenic potential. VEGF supplementation partially recovered the activity impaired by Cx43 down-regulation. In conclusion, reduced Cx43 expression per se in the EPC causes decreased expression of VEGF and impaired angiogenic potential of the cells. Prevention of Cx43 reduction is a potential target to maintain the angiogenic potential of the EPC.
引用
收藏
页码:553 / 560
页数:8
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