Effect of CXCR4 over-expressed endothelial progenitor cells on migration and proliferation in vascular smooth muscle cells

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Effect of CXCR4 over-expressed endothelial progenitor cells on migration and proliferation in vascular smooth muscle cells

Basic Medicine | 更新时间：2026-01-09

- Effect of CXCR4 over-expressed endothelial progenitor cells on migration and proliferation in vascular smooth muscle cells
- Journal of Third Military Medical University Vol. 39, Issue 15, Pages: 1562-1568(2017)
- 作者机构：
  
  400014 重庆，重庆医科大学附属儿童医院心内科，儿科发育疾病研究教育部重点实验室，儿童发育重大疾病国家国际科技合作基地，儿科学重庆市重点实验室
- 作者简介：
- 基金信息：
  
  the National Natural Science Foundation for Young Scholars of China(81301300);the Special Project of Social Undertakings and Livelihood Security of Chongqing Science and Technology Commission(cstc2016shmszx130009)
- DOI：10.16016/j.1000-5404.201701141
  CLC： R322.12;R329.28;R394.2
- Received：25 January 2017，
  
  Revised：2017-04-15，
  
  Published：15 August 2017
- 稿件说明：
移动端阅览
Cancan HE, Xiaojuan JI, Gengsheng YU, et al. Effect of CXCR4 over-expressed endothelial progenitor cells on migration and proliferation in vascular smooth muscle cells[J]. Journal of Third Military Medical University, 2017, 39(15): 1562-1568.
DOI：

Cancan HE, Xiaojuan JI, Gengsheng YU, et al. Effect of CXCR4 over-expressed endothelial progenitor cells on migration and proliferation in vascular smooth muscle cells[J]. Journal of Third Military Medical University, 2017, 39(15): 1562-1568. DOI： 10.16016/j.1000-5404.201701141.

摘要

目的

2

研究过表达趋化因子受体4(chemokine receptor 4，CXCR4) 的内皮祖细胞(endothelial progenitor cells，EPCs)对血管平滑肌细胞(vascular smooth muscle cells，VSMCs)迁移、增殖的影响。

方法

2

分离培养并鉴定大鼠骨髓来源EPCs。CXCR4的重组腺病毒感染EPCs后，流式细胞术、实时荧光定量PCR(qRT-PCR)分别检测细胞膜CXCR4受体及mRNA表达，CCK-8法、Transwell法分别检测EPCs增殖活性、迁移能力。建立过表达CXCR4的EPCs与VSMCs非接触共培养模型，Transwell法、CCK-8法检测EPCs对VSMCs的迁移、细胞存活的影响。

结果

2

CXCR4重组腺病毒感染EPCs 48 h后，EPCs细胞膜CXCR4受体和mRNA表达明显增高(

P

<

0.01)，过表达CXCR4对EPCs增殖活性无明显影响，但可增强EPCs定向迁移能力(

P

<

0.01)。共培养模型中，SDF-1α诱导下，CXCR4组VSMCs迁移、细胞存活率明显降低(

P

<

0.05)，无SDF-1α诱导下空白对照组、GFP组及CXCR4组VSMCs的迁移、细胞存活率整体高于SDF-1α诱导下各组(

P

<

0.05)。

结论

2

过表达CXCR4可增强EPCs的迁移能力，在SDF-1/ CXCR4调控轴中加强EPCs对VSMCs迁移和增殖的抑制作用，可用于防治血管再狭窄的细胞治疗。

Abstract

Objective

2

To determine the effects of endothelial progenitor cells (EPCs) with over-expression of chemokine receptor 4 (CXCR4) on the migration and proliferation of vascular smooth muscle cells (VSMCs).

Methods

2

EPCs were isolated from rat bone marrow

and cultivated and identified

and then were infected with recombinant adenovirus of CXCR4. Flow cytometry and qRT-PCR were used to detect the membrane expression of CXCR4 receptor and the mRNA expression of the molecule respectively. CCK-8 assay was applied to detect the proliferation of EPCs

and Transwell assay was carried out to evaluate the migration of EPCs. Transwell culture plate was constructed into a non-contact co-culture model between CXCR4 over-expressed EPCs and VSMCs. EPCs' effects on the migration of VSMCs and cell survival were detected with Transwell chamber test and CCK-8 assay.

Results

2

After the EP

Cs were infected with recombinant adenovirus of CXCR4 for 48 h

the expression of membrane CXCR4 receptor and CXCR4 mRNA was significantly increased (

P

<

0.01)

and the over-expression of CXCR4 had no significant effect on the proliferative activity of EPCs

but enhanced the oriented migration ability of EPCs (

P

<

0.01). In the co-culture model

the migration and cell viability of VSMCs were obviously lower after the induction of SDF-1a (

P

<

0.05). In absence of SDF-1a induction

the migration and cell viability were obviously higher in the blank control cells

GFP infected cells and CXCR4 over-expressed cells than the corresponding cells after induction of SDF-1a (

P

<

0.05).

Conclusion

2

The over-expression of CXCR4 could increase the migration ability of EPCs

and enhance its inhibitory effects on the migration and proliferation of VSMCs through SDF-1/CXCR4 axis. So it can be used for cell therapy in the prevention and control of vascular restenosis.

关键词

Keywords

references

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