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睡眠蛋白1抑制内皮祖细胞的增殖和管腔形成。

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

作者信息

Kuang Chun-yan, Yang Tian-he, Zhang Yang, Zhang Lu, Wu Qiang

机构信息

Department of Cardiovascular Diseases, The People's Hospital of Guizhou Province, Nanming District, Guiyang, People's Republic of China.

Medical examination center, The People's Hospital of Guizhou Province, Nanming District, Guiyang, People's Republic of China.

出版信息

PLoS One. 2014 Oct 16;9(10):e109711. doi: 10.1371/journal.pone.0109711. eCollection 2014.

DOI:10.1371/journal.pone.0109711
PMID:25329797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4199616/
Abstract

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.

摘要

内皮祖细胞(EPCs)是再内皮化过程中恢复内皮的主要细胞来源。本研究旨在探讨 Schlafen 1(Slfn1)对体内 EPCs 增殖和管腔形成是否有影响。Slfn1 在大鼠 EPCs 中表达。Slfn1 的过表达抑制了 EPCs 的增殖和管腔形成;相反,shRNA 敲低 Slfn1 则促进了 EPCs 的增殖和管腔形成。此外,当 Slfn1 过表达时,EPCs 停滞在细胞周期的 G1 期。相比之下,当 Slfn1 被敲低时,EPCs 进入细胞周期的 S 期。另外,Slfn1 的过表达降低了细胞周期蛋白 D1(Cyclin D1)的表达,而 Slfn1 的敲低则增加了 Cyclin D1 的表达;这些发现表明在 Slfn1 介导的 EPC 增殖中,Cyclin D1 是 Slfn1 的下游分子。综上所述,这些结果表明 Slfn1 在调节 EPC 生物学行为中起关键作用,这可能为再内皮化过程中 EPCs 的应用提供一个新的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a00/4199616/976f41f60225/pone.0109711.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a00/4199616/2adcf6ab154c/pone.0109711.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a00/4199616/976609f79f2b/pone.0109711.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a00/4199616/43e457a31da9/pone.0109711.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a00/4199616/976f41f60225/pone.0109711.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a00/4199616/2adcf6ab154c/pone.0109711.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a00/4199616/976609f79f2b/pone.0109711.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a00/4199616/43e457a31da9/pone.0109711.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a00/4199616/976f41f60225/pone.0109711.g004.jpg

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