Schlafen 1 inhibits the proliferation and tube formation of endothelial progenitor cells.

Schlafen 1 inhibits the proliferation and tube formation of endothelial progenitor cells.
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Schlafen 1 抑制内皮祖细胞的增殖和管形成

DOI:
10.1371/journal.pone.0109711
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Wu Q
Wu Q
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Kuang CY;Yang TH;Zhang Y;Zhang L;Wu Q

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内皮祖细胞(EPCs)是在再内皮化过程中修复内皮的主要细胞来源。本研究旨在探讨Schlafen 1 (Slfn1)是否对EPCs的增殖和成管有影响。Slfn1在大鼠EPCs中表达。Slfn1过表达抑制EPCs的增殖和成管;相反,shRNA敲低Slfn1可促进EPCs的增殖和成管。此外,当Slfn1过表达时,EPCs在细胞周期的G1期被阻滞。相反,当Slfn1被敲除时,EPCs进入细胞周期的S期。Slfn1过表达可降低Cyclin D1的表达,而Slfn1敲低可提高Cyclin D1的表达;这些发现表明Cyclin D1在Slfn1介导的EPC增殖中处于Slfn1的下游。综上所述,这些结果表明Slfn1在EPC生物学行为的调控中发挥了关键作用,这可能为再内皮化过程中EPCs的使用提供了新的靶点。
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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