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血管生成素-2损害与抑制巨噬细胞浸润相关的小鼠后肢缺血侧支动脉生长。

Angiopoietin-2 impairs collateral artery growth associated with the suppression of the infiltration of macrophages in mouse hindlimb ischaemia.

作者信息

Tan Xiaoyong, Yan Kai, Ren Meiping, Chen Ni, Li Yongjie, Deng Xin, Wang Liqun, Li Rong, Luo Mao, Liu Yong, Liu Yan, Wu Jianbo

机构信息

Drug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.

Laboratory for Cardiovascular Pharmacology of Department of Pharmacology, The School of Pharmacy, Southwest Medical University, Luzhou, Sichuan, China.

出版信息

J Transl Med. 2016 Oct 26;14(1):306. doi: 10.1186/s12967-016-1055-x.

DOI:10.1186/s12967-016-1055-x
PMID:27784306
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5080762/
Abstract

BACKGROUND

Angiopoietin-2 (Ang-2), a ligand of the Tie-2 receptor, plays an important role in maintaining endothelial cells and in destabilizing blood vessels. Collateral artery growth (arteriogenesis) is a key adaptive response to arterial occlusion. It is unknown whether the destabilization of blood vessels by Ang-2 can affect arteriogenesis and modulate mononuclear cell function. This study aimed to investigate the effects of Ang-2 on collateral artery growth.

METHODS

Hindlimb ischaemia model was produced in C57BL/6 mice by femoral artery ligation. Blood flow perfusion was measured using a laser Doppler perfusion imager quantitative RT-PCR analysis was applied to identify the level of angiogenic factors.

RESULTS

After the induction of hindlimb ischaemia, blood flow recovery was impaired in mice treated with recombinant Ang-2 protein; this was accompanied by a reduction of peri-collateral macrophage infiltration. In addition, quantitative RT-PCR analysis revealed that Ang-2 treatment decreased monocyte chemotactic protein-1 (MCP-1), platelet-derived growth factor-BB (PDGF-BB) mRNA levels in ischaemic adductor muscles. Ang-2 can lead to macrophage M1/M2 polarization shift inhibition in the ischaemic muscles. Furthermore, Ang-2 reduced the in vitro inflammatory response in macrophages and vascular cells involved in arteriogenesis.

CONCLUSIONS

Our results demonstrate that Ang-2 is essential for efficient arteriogenesis, which controls macrophage infiltration.

摘要

背景

血管生成素-2（Ang-2）是Tie-2受体的配体，在维持内皮细胞和使血管不稳定方面发挥重要作用。侧支动脉生长（动脉生成）是对动脉闭塞的关键适应性反应。尚不清楚Ang-2导致的血管不稳定是否会影响动脉生成并调节单核细胞功能。本研究旨在探讨Ang-2对侧支动脉生长的影响。

方法

通过结扎股动脉在C57BL/6小鼠中建立后肢缺血模型。使用激光多普勒灌注成像仪测量血流灌注，应用定量逆转录聚合酶链反应（RT-PCR）分析来确定血管生成因子的水平。

结果

诱导后肢缺血后，用重组Ang-2蛋白处理的小鼠血流恢复受损；这伴随着侧支周围巨噬细胞浸润的减少。此外，定量RT-PCR分析显示，Ang-2处理降低了缺血内收肌中单核细胞趋化蛋白-1（MCP-1）、血小板衍生生长因子-BB（PDGF-BB）的mRNA水平。Ang-2可导致缺血肌肉中巨噬细胞M1/M2极化转变受到抑制。此外，Ang-2降低了参与动脉生成的巨噬细胞和血管细胞的体外炎症反应。

结论

我们的结果表明，Ang-2对于有效的动脉生成至关重要，它控制着巨噬细胞浸润。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9603/5080762/ffde26adf790/12967_2016_1055_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9603/5080762/1d68b7eb21f6/12967_2016_1055_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9603/5080762/83266f284a4f/12967_2016_1055_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9603/5080762/ba7224fdd138/12967_2016_1055_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9603/5080762/ffde26adf790/12967_2016_1055_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9603/5080762/1d68b7eb21f6/12967_2016_1055_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9603/5080762/83266f284a4f/12967_2016_1055_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9603/5080762/ba7224fdd138/12967_2016_1055_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9603/5080762/ffde26adf790/12967_2016_1055_Fig4_HTML.jpg

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