首页> 外文期刊>Acta ophthalmologica Scandinavica >Delayed neovascularization in inflammation-induced corneal neovascularization in interleukin-10-deficient mice
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Delayed neovascularization in inflammation-induced corneal neovascularization in interleukin-10-deficient mice

机译:白细胞介素10缺乏症小鼠炎症诱导的角膜新血管形成中的延迟新血管形成

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Purpose: To investigate the potential modulatory role of interleukin-10 (IL-10) in the suture model for corneal neovascularization. Methods: Neovascularized areas were measured on corneal flat-mounts in IL-10~(-/-) and wild-type C57BL6 mice. The inflammatory cellular response was characterized with immunohistochemistry. Gene expression was measured by real-time polymerase chain reaction. Results: IL-10~(-/-) mice showed a delayed neovascular response compared to wild-type animals at day 6 after suture, when approximately half of the cornea was neovascularized. No apparent differences in inflammatory responses or in messenger RNA (mRNA) expression for proangiogenic factors were detected in IL-10~(-/-) versus wild-type mice. Conclusion: IL-10 appears to have a proangiogenic effect in the suture model for corneal neovascularization that cannot be explained by either IL-10's anti-inflammatory effect or apparent cross-talk with the angiogenic factors vascular endothelial growth factor (VEGF)-A, metalloproteinase (MMP)-2 and MMP-9, angiopoietin (Ang)-1 and Ang-2.
机译:目的:研究白细胞介素10(IL-10)在角膜新生血管缝合模型中的潜在调节作用。方法:在IL-10〜(-/-)和野生型C57BL6小鼠的角膜平台上测量新生血管面积。用免疫组织化学表征炎性细胞反应。通过实时聚合酶链反应测量基因表达。结果:与野生型动物相比,IL-10〜(-/-)小鼠在缝合后第6天显示出较晚的新生血管反应,此时约有一半的角膜新生血管。与野生型小鼠相比,IL-10〜(-/-)小鼠的炎症反应或促血管生成因子的信使RNA(mRNA)表达没有明显差异。结论:IL-10在缝线模型的角膜新生血管中似乎具有促血管生成作用,而不能通过IL-10的抗炎作用或与血管生成因子血管内皮生长因子(VEGF)-A的明显串扰来解释,金属蛋白酶(MMP)-2和MMP-9,血管生成素(Ang)-1和Ang-2。

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