共 22 条
Schlafen 1 Inhibits the Proliferation and Tube Formation of Endothelial Progenitor Cells
被引:21
作者:

Kuang, Chun-yan
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h-index: 0
机构:
Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China

Yang, Tian-he
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h-index: 0
机构:
Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China

Zhang, Yang
论文数: 0 引用数: 0
h-index: 0
机构:
Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China

Zhang, Lu
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机构:
Peoples Hosp Guizhou Prov, Med Examinat Ctr, Guiyang, Peoples R China Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China

Wu, Qiang
论文数: 0 引用数: 0
h-index: 0
机构:
Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China
机构:
[1] Peoples Hosp Guizhou Prov, Dept Cardiovasc Dis, Guiyang, Peoples R China
[2] Peoples Hosp Guizhou Prov, Med Examinat Ctr, Guiyang, Peoples R China
来源:
基金:
美国国家卫生研究院;
中国国家自然科学基金;
关键词:
CYCLIN D1;
FAMILY;
GENE;
ARREST;
GROWTH;
LOCALIZATION;
ACTIVATION;
EXPRESSION;
MIGRATION;
D O I:
10.1371/journal.pone.0109711
中图分类号:
O [数理科学和化学];
P [天文学、地球科学];
Q [生物科学];
N [自然科学总论];
学科分类号:
07 ;
0710 ;
09 ;
摘要:
Endothelial progenitor cells (EPCs) are the major source of cells that restore the endothelium during reendothelialization. This study was designed to investigate whether Schlafen 1 (Slfn1) has an effect on the proliferation and tube formation of EPCs in vivo. Slfn1 was expressed in rat EPCs. The overexpression of Slfn1 suppressed the proliferation and tube formation of EPCs; conversely, the knockdown of Slfn1 by shRNA promoted the proliferation and tube formation of EPCs. Furthermore, when Slfn1 was overexpressed, the EPCs were arrested in the G1 phase of the cell cycle. In contrast, when Slfn1 was knocked down, the EPCs progressed into the S phase of the cell cycle. Additionally, the overexpression of Slfn1 decreased the expression of Cyclin D1, whereas the knockdown of Slfn1 increased the expression of Cyclin D1; these findings suggest that Cyclin D1 is downstream of Slfn1 in Slfn1-mediated EPC proliferation. Taken together, these results indicate a key role for Slfn1 in the regulation of EPC biological behavior, which may provide a new target for the use of EPCs during reendothelialization.
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