Silencing stromal interaction molecule 1 by RNA interference inhibits the proliferation and migration of endothelial progenitor cells

Silencing stromal interaction molecule 1 by RNA interference inhibits the proliferation and migration of endothelial progenitor cells
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RNA干扰沉默基质相互作用分子1抑制内皮祖细胞的增殖和迁移

DOI:
10.1016/j.bbrc.2010.06.088
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发表时间:
2010-07-23
影响因子:
3.1
通讯作者:
Huang, Lan
Huang, Lan
中科院分区:
生物学4区
文献类型:
--
作者:
Kuang, Chun-yan;Yu, Yang;Huang, Lan

文献摘要

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下调基质相互作用分子1 (STIM1)可显著抑制血管损伤后新生内膜增生。内皮祖细胞(EPCs)是响应内皮修复的主要细胞来源,并通过减少血管损伤后新内膜的形成来促进再内皮化。我们假设STIM1对新生内膜增生抑制的作用是通过其对EPCs生物学特性的影响来介导的。在这项研究中,我们研究了STIM1对EPCs增殖和迁移的影响,并利用培养的大鼠骨髓来源的EPCs检测了STIM1敲除的影响。STIM1在EPCs中表达,通过腺病毒递送小干扰RNA (siRNA)敲低STIM1可显著抑制EPCs的增殖和迁移。此外,转染后48小时,STIM1敲除减少了储存操作的通道进入。补充重组人STIM1逆转了STIM1敲低的作用。我们的数据表明,储存操作的瞬时受体电位规范1通道通过STIM1参与调节EPCs的生物学特性。STIM1是大鼠EPCs细胞增殖和迁移的有效调节剂,可能在EPCs的生物学特性中发挥重要作用。(C) 2010爱思唯尔公司版权所有。
Knockdown of stromal interaction molecule 1 (STIM1) significantly suppresses neointima hyperplasia after vascular injury. Endothelial progenitor cells (EPCs) are the major source of cells that respond to endothelium repair and contribute to re-endothelialization by reducing neointima formation after vascular injury. We hypothesized that the effect of STIM1 on neointima hyperplasia inhibition is mediated through its effect on the biological properties of EPCs. In this study, we investigated the effects of STIM1 on the proliferation and migration of EPCs and examined the effect of STIM1 knockdown using cultured rat bone marrow-derived EPCs. STIM1 was expressed in EPCs, and knockdown of STIM1 by adenoviral delivery of small interfering RNA (siRNA) significantly suppressed the proliferation and migration of EPCs. Furthermore, STIM1 knockdown decreased store-operated channel entry 48 h after transfection. Replenishment with recombinant human STIM1 reversed the effects of STIM1 knockdown. Our data suggest that the store-operated transient receptor potential canonical 1 channel is involved in regulating the biological properties of EPCs through STIM1. STIM1 is a potent regulator of cell proliferation and migration in rat EPCs and may play an important role in the biological properties of EPCs. (C) 2010 Elsevier Inc. All rights reserved.