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玻璃体糖蛋白 opticin 抑制视网膜前新生血管。

The vitreous glycoprotein opticin inhibits preretinal neovascularization.

机构信息

School of Biomedicine, University of Manchester, UK.

出版信息

Invest Ophthalmol Vis Sci. 2012 Jan 25;53(1):228-34. doi: 10.1167/iovs.11-8514.

DOI:10.1167/iovs.11-8514
PMID:22159013
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3292360/
Abstract

PURPOSE

Opticin is an extracellular matrix glycoprotein that the authors discovered in the vitreous humor of the eye. It is synthesized by the nonpigmented ciliary epithelium and secreted into the vitreous cavity and, unusually for an extracellular matrix molecule, high-level synthesis is maintained into adult life. Here the authors investigated the hypothesis that opticin influences vascular development in the posterior segment of the eye and pathologic angiogenesis into the normally avascular, mature (secondary) vitreous.

METHODS

Opticin was localized in murine eyes by immunohistochemistry. An opticin knockout mouse was established and vascular development was compared between knockout and wild-type mice. Wild-type and opticin null mice were compared in the oxygen-induced retinopathy model, a model of pathologic angiogenesis, and this model was also used to assess the effects of intravitreal injection of recombinant opticin into eyes of wild-type mice.

RESULTS

Opticin colocalizes with the collagen type II-rich fibrillar network of the vitreous, the inner limiting lamina, the lens capsule, the trabecular meshwork, and the iris. Analyses of the hyaloid and retinal vasculature showed that opticin has no effect on hyaloid vascular regression or developmental retinal vascularization. However, using the oxygen-induced retinopathy model, the authors demonstrated that opticin knockout mice produce significantly more preretinal neovascularization than wild-type mice, and the intravitreal delivery of excess opticin inhibited the formation of neovessels in wild-type mice.

CONCLUSIONS

A lack of opticin does not influence vascular development, but opticin is antiangiogenic and inhibits preretinal neovascularization.

摘要

目的

Opticin 是一种细胞外基质糖蛋白,作者在眼睛的玻璃体中发现了它。它由非色素睫状上皮细胞合成,并分泌到玻璃体腔中,而且不同寻常的是,作为一种细胞外基质分子,高水平的合成一直维持到成年。在这里,作者研究了这样一个假设,即 Opticin 影响眼睛后节的血管发育和病理性血管生成进入正常无血管的成熟(次级)玻璃体。

方法

作者通过免疫组织化学法定位了小鼠眼中的 Opticin。建立了 Opticin 敲除小鼠,并比较了敲除和野生型小鼠之间的血管发育情况。作者比较了野生型和 Opticin 缺失型小鼠在氧诱导的视网膜病变模型中的情况,该模型是一种病理性血管生成模型,并且还使用该模型评估了向野生型小鼠的玻璃体中注射重组 Opticin 的效果。

结果

Opticin 与玻璃体中富含 II 型胶原的纤维状网络、内界膜、晶状体囊、小梁网和虹膜共定位。对玻璃体液和视网膜血管的分析表明,Opticin 对玻璃体液血管的退化或发育性视网膜血管化没有影响。然而,使用氧诱导的视网膜病变模型,作者证明 Opticin 敲除小鼠比野生型小鼠产生更多的视网膜前新生血管,并且向野生型小鼠玻璃体中注射过量 Opticin 可抑制新血管的形成。

结论

缺乏 Opticin 不会影响血管发育,但 Opticin 具有抗血管生成作用,并抑制视网膜前新生血管形成。

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