趋化因子配体5通过诱导巨噬细胞极化促进主动脉夹层发生

袁铭; 王乐

doi:10.14188/j.1671-8852.22024.0148

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趋化因子配体5通过诱导巨噬细胞极化促进主动脉夹层发生

基础及临床医学研究 | 更新时间：2026-11-05

- 趋化因子配体5通过诱导巨噬细胞极化促进主动脉夹层发生
- C‑C motif chemokine ligand 5 promotes aortic dissection by inducing macrophage polarization
- 武汉大学学报（医学版） 2025年46卷第4期页码：463-468
- 作者机构：
  
  武汉大学中南医院心血管外科/心脏大血管外科微创诊疗湖北省工程研究中心/武汉市结构性心脏病微创诊疗临床医学研究中心湖北武汉 430071
- 作者简介：
  
  袁铭，男，1998—，医学硕士生，主要从事心血管相关疾病的基础研究， E‑mail：mingyuan@whu.edu.cn
  王乐，男，1965—，副主任医师，主要从事心血管外科的临床、科研及教学研究， E‑mail：wangleznh@126.com
- 基金信息：
  
  国家自然科学基金资助项目(82200534)
- DOI：10.14188/j.1671-8852.22024.0148
  中图分类号： R34
- 收稿：2024-03-04，
  
  纸质出版：2025-04-25
- 稿件说明：
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袁铭,王乐.趋化因子配体5通过诱导巨噬细胞极化促进主动脉夹层发生[J].武汉大学学报（医学版）,2025,46(04):463-468.

YUAN Ming,WANG Le.C‑C motif chemokine ligand 5 promotes aortic dissection by inducing macrophage polarization[J].Medical Journal of Wuhan University,2025,46(04):463-468.
袁铭,王乐.趋化因子配体5通过诱导巨噬细胞极化促进主动脉夹层发生[J].武汉大学学报（医学版）,2025,46(04):463-468. DOI： 10.14188/j.1671-8852.22024.0148.

YUAN Ming,WANG Le.C‑C motif chemokine ligand 5 promotes aortic dissection by inducing macrophage polarization[J].Medical Journal of Wuhan University,2025,46(04):463-468. DOI： 10.14188/j.1671-8852.22024.0148.

摘要

目的

探究趋化因子配体5（CCL5）在主动脉夹层（AD）发生发展中的作用。

方法

收集临床健康主动脉组织（来自临床健康捐献者）及夹层主动脉组织(来自AD患者)进行检测。使用3周龄C57BL/6小鼠分别喂食含或不含0.25%氨基丙腈（BAPN）的纯净水2周，并继续观察2周后，收集主动脉样本进行检测。使用原代细胞提取、蛋白质免疫印迹、实时荧光定量PCR、免疫荧光技术探究CCL5在AD发生中的作用。

结果

相较于正常主动脉组织，CCL5在AD患者及小鼠AD模型的主动脉组织中，蛋白及mRNA表达上调；免疫荧光证实CCL5与M1型巨噬细胞共定位；体外实验证实CCL5通过CCR1受体促进小鼠骨髓原代巨噬细胞M1极化。

结论

CCL5可能通过作用于CCR1受体诱导巨噬细胞向M1方向极化从而诱导AD的发生。

Abstract

Objective

To investigate the role of CCL5 in the development and progression of aortic dissection (AD).

Methods

The healthy aortic tissues (from clinical health donors) and aortic tissues with AD (from patients with AD) were collected clinically for testing. Three⁃week‑old C57BL/6 mice were fed with purified water containing or without 0.25% aminoacetonitrile (BAPN) for two weeks and were observed for two weeks before collecting aortic samples for testing. The effects of CCL5 on the development of AD were explored using primary cell extraction

protein immunoblotting

real‑time fluorescence quantitative PCR

and immunofluorescence.

Results

Compared with those in normal aortic tissues

CCL5 protein and mRNA expression were upregulated in the aortic tissue of AD patients and mouse AD models; Immunofluorescence confirmed co⁃localization of CCL5 with M1 macrophages;

In vitro

experiments confirmed that CCL5 promoted M1 polarization of primary mouse bone marrow⁃derived macrophages through

the CCR1 receptor.

Conclusion

CCL5 might induce macrophage polarization towards the M1 direction

thus inducing the occurrence of AD.

关键词

Keywords

references

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