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基因敲除趋化因子受体 Ccr6 可减少载脂蛋白 E 缺陷小鼠的动脉粥样硬化形成。

Genetic deletion of chemokine receptor Ccr6 decreases atherogenesis in ApoE-deficient mice.

机构信息

Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Circ Res. 2011 Aug 5;109(4):374-81. doi: 10.1161/CIRCRESAHA.111.242578. Epub 2011 Jun 16.

DOI:10.1161/CIRCRESAHA.111.242578
PMID:21680896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3151346/
Abstract

RATIONALE

The chemokine receptor Ccr6 is a G-protein-coupled receptor expressed on various types of leukocytes identified in mouse atherosclerotic lesions. Recent evidence suggests that both CCR6 and its ligand CCL20 are also present in human atheroma; however, their functional roles in atherogenesis remain undefined.

OBJECTIVE

Our objective was to delineate the role of Ccr6 in atherogenesis in the apolipoprotein E-deficient (ApoE(-/-)) mouse model of atherosclerosis.

METHODS AND RESULTS

Both Ccr6 and Ccl20 are expressed in atherosclerotic aorta from ApoE(-/-) mice. Aortic lesion area in Ccr6(-/-)ApoE(-/-) mice was ∼40% and ∼30% smaller than in Ccr6(+/+)ApoE(-/-) mice at 16 and 24 weeks of age, respectively. Transplantation of bone marrow from Ccr6(-/-) mice into ApoE(-/-) mice resulted in ∼40% less atherosclerotic lesion area than for bone marrow from Ccr6(+/+) mice; lesions in Ccr6(-/-)ApoE(-/-) mice had 44% less macrophage content than lesions in Ccr6(+/+)ApoE(-/-) mice. Ccr6 was expressed on a subset of primary mouse monocytes. Accordingly, Ccl20 induced chemotaxis of primary monocytes from wild-type but not Ccr6(-/-) mice; moreover, Ccl20 induced monocytosis in ApoE(-/-) mice in vivo. Consistent with this, we observed 30% fewer monocytes in circulating blood of Ccr6(-/-)ApoE(-/-) mice, mainly because of fewer CD11b(+)Ly6C(high) inflammatory monocytes.

CONCLUSIONS

Ccr6 promotes atherosclerosis in ApoE-deficient mice, which may be due in part to Ccr6 support of normal monocyte levels in blood, as well as direct Ccr6-dependent monocyte migration.

摘要

背景

趋化因子受体 Ccr6 是一种 G 蛋白偶联受体，存在于小鼠动脉粥样硬化病变中各种类型的白细胞上。最近的证据表明，CCR6 及其配体 CCL20 也存在于人类动脉粥样硬化斑块中；然而，其在动脉粥样硬化形成中的功能作用仍未确定。

目的

本研究旨在描述趋化因子受体 Ccr6 在载脂蛋白 E 缺陷（ApoE(-/-)）小鼠动脉粥样硬化模型中的动脉粥样硬化形成中的作用。

方法和结果

在 ApoE(-/-)小鼠的动脉粥样硬化主动脉中均表达 Ccr6 和 Ccl20。与 Ccr6(+/+)ApoE(-/-)小鼠相比，16 周和 24 周龄 Ccr6(-/-)ApoE(-/-)小鼠的主动脉病变面积分别减少约 40%和 30%。将 Ccr6(-/-)小鼠的骨髓移植到 ApoE(-/-)小鼠中，导致动脉粥样硬化病变面积比 Ccr6(+/+)骨髓移植减少约 40%；Ccr6(-/-)ApoE(-/-)小鼠的病变中巨噬细胞含量比 Ccr6(+/+)ApoE(-/-)小鼠的病变少 44%。Ccr6 在一组原代小鼠单核细胞上表达。因此，Ccl20 诱导来自野生型而非 Ccr6(-/-)小鼠的原代单核细胞趋化；此外，Ccl20 在体内诱导 ApoE(-/-)小鼠单核细胞增多症。与此一致，我们观察到 Ccr6(-/-)ApoE(-/-)小鼠循环血液中的单核细胞减少 30%，主要是由于 CD11b(+)Ly6C(high)炎症性单核细胞减少。

结论

Ccr6 促进 ApoE 缺陷型小鼠的动脉粥样硬化形成，这可能部分归因于 Ccr6 对血液中正常单核细胞水平的支持，以及 Ccr6 依赖性单核细胞的直接迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/34ebe37a7561/nihms310510f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/47ca682266bb/nihms310510f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/69d517cb6fed/nihms310510f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/dadeab32d574/nihms310510f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/13631a6b0e5b/nihms310510f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/34ebe37a7561/nihms310510f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/47ca682266bb/nihms310510f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/7bfe87127c55/nihms310510f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/69d517cb6fed/nihms310510f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/dadeab32d574/nihms310510f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/13631a6b0e5b/nihms310510f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5de/3151346/34ebe37a7561/nihms310510f6.jpg

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