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首页> 外文期刊>Cornea >Opposite roles of CCR2 and CX3CR1 macrophages in alkali-induced corneal neovascularization.
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Opposite roles of CCR2 and CX3CR1 macrophages in alkali-induced corneal neovascularization.

机译：CCR2和CX3CR1巨噬细胞在碱诱导的角膜新生血管形成中的作用相反。

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PURPOSE: The purpose of this study was to investigate the role of infiltrating macrophages in the development of experimental corneal neovascularization. METHODS: Corneal neovascularization was induced by alkali injury in mice deficient in a macrophage-tropic chemokine receptor, CCR2 or CX3CR1, or in mice treated with clodronate-liposomes (Cl2MDP-lip), which can selectively deplete monocytes/macrophages. Corneal neovascularization 2 weeks after alkali injury was assessed by immunostaining with anti-CD31 antibody. Intracorneal expression of proangiogenic and antiangiogenic factors was determined by reverse transcription-polymerase chain reaction. RESULTS: CCR2-deficient mice exhibited reduced alkali-induced corneal neovascularization with reduced macrophage infiltration, whereas CX3CR1-deficient mice developed a more severe form of alkali-induced corneal neovascularization with reduced macrophage infiltration. Selective macrophage depletion by Cl2MDP-lip treatment failed to affect alkali-induced corneal neovascularization as evidenced by immunohistochemical analysis using anti-CD31 antibody, whereas intracorneal macrophage infiltration was markedly reduced. Alkali injury enhanced the expression of proangiogenic molecules, including matrix metalloproteinase-2, matrix metalloproteinase-9, and tumor necrosis factor alpha, and antiangiogenic factors, including a disintegrin and metalloprotease with thrombospondin (ADAMTS)-1, thrombospondin-1, and thrombospondin-2. Cl2MDP-lip-treated mice exhibited a reduction in the messenger RNA expression of these molecules. CONCLUSION: Because CCR2- and CX3CR1-expressing macrophages exhibit opposite activities in angiogenesis, depletion of macrophages as a whole may not have apparent effects on alkali-induced corneal neovascularization.
机译：目的：本研究的目的是研究浸润性巨噬细胞在实验性角膜新生血管形成中的作用。方法：在缺乏巨噬细胞趋化因子受体CCR2或CX3CR1的小鼠中，或在可选择性消耗单核细胞/巨噬细胞的氯膦酸盐脂质体（Cl2MDP-lip）治疗的小鼠中，碱损伤引起角膜新生血管形成。通过抗CD31抗体免疫染色评估碱损伤后2周的角膜新生血管形成。通过逆转录-聚合酶链反应确定促血管生成因子和抗血管生成因子的角膜内表达。结果：CCR2缺陷小鼠表现出减少的碱诱导角膜新生血管形成，而巨噬细胞浸润减少，而CX3CR1缺陷小鼠表现出更严重的碱诱导的角膜新生血管形成，而巨噬细胞浸润减少。使用抗CD31抗体的免疫组织化学分析表明，通过Cl2MDP-lip处理的选择性巨噬细胞耗竭未能影响碱诱导的角膜新生血管形成，而角膜内巨噬细胞浸润却明显减少。碱损伤增强了促血管生成分子的表达，包括基质金属蛋白酶-2，基质金属蛋白酶9和肿瘤坏死因子α，以及抗血管生成因子，包括具有血小板反应蛋白（ADAMTS）-1，血小板反应蛋白-1和血小板反应蛋白-的整合素和金属蛋白酶。 2。 Cl2MDP-嘴唇治疗的小鼠表现出这些分子的信使RNA表达的减少。结论：由于表达CCR2和CX3CR1的巨噬细胞在血管生成中具有相反的活性，因此从整体上看，巨噬细胞的耗竭可能对碱诱导的角膜新生血管没有明显的影响。

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