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一种新型的穿刺诱导虹膜新生血管形成的体内模型。

A novel in vivo model of puncture-induced iris neovascularization.

作者信息

Beaujean Ophélie, Locri Filippo, Aronsson Monica, Kvanta Anders, André Helder

机构信息

Department of Clinical Neuroscience, Section of Eye and Vision, St. Erik Eye Hospital, Karolinska Institutet, Stockholm, Sweden.

出版信息

PLoS One. 2017 Jun 28;12(6):e0180235. doi: 10.1371/journal.pone.0180235. eCollection 2017.

DOI:10.1371/journal.pone.0180235
PMID:28658313
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5489193/
Abstract

PURPOSE

To assess iris neovascularization by uveal puncture of the mouse eye and determine the role of angiogenic factors during iris neovascularization.

METHODS

Uveal punctures were performed on BalbC mouse eyes to induce iris angiogenesis. VEGF-blockage was used as an anti-angiogenic treatment, while normoxia- and hypoxia-conditioned media from retinal pigment epithelium (RPE) cells was used as an angiogenic-inducer in this model. Iris vasculature was determined in vivo by noninvasive methods. Iris blood vessels were stained for platelet endothelial cell adhesion molecule-1 and vascular sprouts were counted as markers of angiogenesis. Expression of angiogenic and inflammatory factors in the puncture-induced model were determined by qPCR and western blot.

RESULTS

Punctures led to increased neovascularization and sprouting of the iris. qPCR and protein analysis showed an increase of angiogenic factors, particularly in the plasminogen-activating receptor and inflammatory systems. VEGF-blockage partly reduced iris neovascularization, and treatment with hypoxia-conditioned RPE medium led to a statistically significant increase in iris neovascularization.

CONCLUSIONS

This study presents the first evidence of a puncture-induced iris angiogenesis model in the mouse. In a broader context, this novel in vivo model of neovascularization has the potential for noninvasive evaluation of angiogenesis modulating substances.

摘要

目的

通过对小鼠眼睛进行脉络膜穿刺来评估虹膜新生血管形成，并确定血管生成因子在虹膜新生血管形成过程中的作用。

方法

对BalbC小鼠眼睛进行脉络膜穿刺以诱导虹膜血管生成。使用VEGF阻断作为抗血管生成治疗，而来自视网膜色素上皮（RPE）细胞的常氧和低氧条件培养基在该模型中用作血管生成诱导剂。通过非侵入性方法在体内确定虹膜脉管系统。对虹膜血管进行血小板内皮细胞粘附分子-1染色，并将血管芽计数作为血管生成的标志物。通过qPCR和蛋白质印迹法确定穿刺诱导模型中血管生成和炎症因子的表达。

结果

穿刺导致虹膜新生血管形成增加和血管芽生。qPCR和蛋白质分析显示血管生成因子增加，特别是在纤溶酶原激活受体和炎症系统中。VEGF阻断部分减少了虹膜新生血管形成，而用低氧条件的RPE培养基处理导致虹膜新生血管形成有统计学意义的增加。

结论

本研究首次证明了小鼠中穿刺诱导的虹膜血管生成模型。在更广泛的背景下，这种新型的体内新生血管形成模型具有对血管生成调节物质进行非侵入性评估的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/c4bdbc0a7e58/pone.0180235.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/60e944af56b5/pone.0180235.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/ff3407546915/pone.0180235.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/5450aeb7bb49/pone.0180235.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/ee5602a92baa/pone.0180235.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/c4bdbc0a7e58/pone.0180235.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/60e944af56b5/pone.0180235.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/ff3407546915/pone.0180235.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/5450aeb7bb49/pone.0180235.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/ee5602a92baa/pone.0180235.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbb/5489193/c4bdbc0a7e58/pone.0180235.g005.jpg

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