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首页> 外文期刊>Investigative ophthalmology & visual science >Role of macrophage migration inhibitory factor in corneal neovascularization.
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Role of macrophage migration inhibitory factor in corneal neovascularization.

机译:巨噬细胞迁移抑制因子在角膜新生血管形成中的作用。

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摘要

PURPOSE: To determine the role of macrophage migration inhibitory factor (MIF) in inflammatory corneal neovascularization. METHODS: Corneal neovascularization was induced by suturing 10-0 nylon 1 mm away from limbal vessel or limbal scraping after 0.15 M NaOH application in BALB/c mice. MIF expression was evaluated by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), Western blot analysis, and immunohistochemistry. To investigate the function of MIF in inflammatory corneal neovascularization, the neovascularized area and number of infiltrating F4/80-positive cells (monocytes/macrophages) were compared between wild-type mice and homozygous MIF-deficient mice. RESULTS: MIF mRNA and protein markedly increased in the neovascularized corneas compared with normal corneas by RT-PCR and Western blot analysis, respectively. MIF expression was upregulated immunohistochemically, not only in the corneal epithelium but also in the stromal infiltrating cells of neovascularized corneas. Neovascularized area in corneas of MIF(-/-) mice was significantly small compared with that in wild-type mice on day 7 after corneal suture and on day 14 after limbal scrape, and MIF(-/-) cornea had approximately 30% less neovascularized area than did wild-type cornea in both models. Neovascularized corneas in MIF-deficient mice had significantly fewer monocytes/macrophages than those in wild-type control mice. CONCLUSIONS: These findings indicate that MIF, abundantly expressed in neovascularized corneas, has an angiogenic role in inflammatory corneal neovascularization and may be a therapeutic target for suppression of corneal neovascularization.
机译:目的:确定巨噬细胞迁移抑制因子(MIF)在炎性角膜新生血管形成中的作用。方法:在BALB / c小鼠中,在距角膜缘血管1mm处缝合10-0尼龙或在刮除角膜缘后刮伤角膜缘,诱导角膜新生血管形成。通过半定量逆转录-聚合酶链反应(RT-PCR),蛋白质印迹分析和免疫组化评估MIF表达。为了研究MIF在炎症性角膜新生血管中的功能,比较了野生型小鼠和纯合MIF缺陷小鼠的新生血管面积和浸润性F4 / 80阳性细胞(单核细胞/巨噬细胞)的数量。结果:RT-PCR和Western blot分析显示,新生血管化角膜中的MIF mRNA和蛋白与正常角膜相比显着增加。不仅在角膜上皮中,而且在新血管化角膜的基质浸润细胞中,MIF表达都通过免疫组织化学上调。 MIF(-/-)小鼠角膜缝合后第7天和角膜缘刮擦后第14天,与野生型小鼠相比,角膜的新生血管面积显着较小,MIF(-/-)角膜的新生血管面积减少了约30%在两个模型中,新血管形成的面积都比野生型角膜的面积大。与野生型对照小鼠相比,MIF缺陷小鼠中的新生血管角膜单核细胞/巨噬细胞明显更少。结论:这些发现表明,在新生血管化角膜中大量表达的MIF在炎症性角膜新生血管中具有血管生成作用,并且可能是抑制角膜新生血管的治疗靶标。

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