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首页> 外文期刊>Ophthalmic Research: Journal for Research in Experimental and Clinical Ophthalmology >Exacerbation of retinal degeneration and choroidal neovascularization induced by subretinal injection of Matrigel in CCL2/MCP-1-deficient mice.
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Exacerbation of retinal degeneration and choroidal neovascularization induced by subretinal injection of Matrigel in CCL2/MCP-1-deficient mice.

机译:视网膜下注射Matrigel对CCL2 / MCP-1缺陷小鼠的视网膜变性和脉络膜新生血管形成的加重。

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摘要

This study presents a mouse model for human age-related macular degeneration (AMD) as characterized by subretinal deposit and choroidal neovascularization. Matrigel, a basement membrane extract, solidifies after implantation in tissue and can stimulate local angiogenesis. This study demonstrates the induction of neovascularization and focal retinal degeneration following subretinal Matrigel injection in mice. In senescent mice, the normal functioning of CC chemokine CCL2/MCP-1 and its receptor CCR2 confers protection against age-related retinal degeneration, a disease that shares many similar features with human AMD. Our data shows that CCL2-deficient mice develop more severe disease as compared to the wild-type controls. These findings suggest that Matrigel subretinal injection could be used to generate AMD-like pathological changes. The data support the previously proposed role of CCL2 in AMD pathogenesis.
机译:这项研究提出了一种以视网膜下沉积和脉络膜新生血管为特征的人类年龄相关性黄斑变性(AMD)小鼠模型。基质膜提取物基质胶(Matrigel)在植入组织后固化,可以刺激局部血管生成。这项研究表明小鼠视网膜下基质胶注射后诱导新生血管形成和局灶性视网膜变性。在衰老小鼠中,CC趋化因子CCL2 / MCP-1及其受体CCR2的正常功能赋予了针对年龄相关性视网膜变性的保护作用,这种疾病与人类AMD具有许多相似的特征。我们的数据表明,与野生型对照相比,缺乏CCL2的小鼠患病更为严重。这些发现表明,Matrigel视网膜下注射可用于产生类似AMD的病理变化。数据支持先前提出的CCL2在AMD发病机理中的作用。

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