Oxygen-induced retinopathy in the mouse.

Oxygen-induced retinopathy in the mouse.
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DOI:
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发表时间:
1994
影响因子:
4.4
通讯作者:
Lois E. H. Smith;Eva Wesoloiuski;Angela McLellan;Sandra K. Kostyk;Robert D'Amato;Richard Sullivan
Lois E. H. Smith;Eva Wesoloiuski;Angela McLellan;Sandra K. Kostyk;Robert D'Amato;Richard Sullivan
中科院分区:
医学2区
文献类型:
--
作者:
Lois E. H. Smith;Eva Wesoloiuski;Angela McLellan;Sandra K. Kostyk;Robert D'Amato;Richard Sullivan

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目的建立可复制、可定量增殖性视网膜新生血管的小鼠视网膜病变模型,为研究早产儿视网膜病变(ROP)及其他血管病变视网膜新生血管的发病机制及治疗干预提供实验依据。方法将1周龄C57BL/6J小鼠暴露于75%氧气中5d,然后暴露于室内空气中。开发了一种新的荧光素-葡聚糖灌注法来评估血管形态。通过在6微米的矢状面上计数从视网膜延伸到玻璃体的新血管的核来量化增殖性新生血管反应。切片进行胶质纤维酸性蛋白(GFAP)染色。结果荧光素-葡聚糖血管造影术显示了整个血管形态,包括平铺型视网膜中的新生血管。高氧诱导的新生血管发生在中周部有血管视网膜和无血管视网膜的交界处。所有仔鼠的视网膜新生血管均发生在出生后第17天至第21天。高氧组9只眼平均每横截面有89个新生血管核,而正常氧对照组8只眼每横截面新生血管核少于1个(P<0.0001)。增殖性血管与GFAP阳性的星形胶质细胞突起无关。结论建立了一种重复性好、可量化的小鼠视网膜新生血管模型,可用于研究视网膜新生血管的发病机制以及药物干预ROP和其他视网膜血管病变的研究。
PURPOSE To develop oxygen-induced retinopathy in the mouse with reproducible and quantifiable proliferative retinal neovascularization suitable for examining pathogenesis and therapeutic intervention for retinal neovascularization in retinopathy of prematurity (ROP) and other vasculopathologies. METHODS One-week-old C57BL/6J mice were exposed to 75% oxygen for 5 days and then to room air. A novel fluorescein-dextran perfusion method has been developed to assess the vascular pattern. The proliferative neovascular response was quantified by counting the nuclei of new vessels extending from the retina into the vitreous in 6 microns sagittal cross-sections. Cross-sections were also stained for glial fibrillary acidic protein (GFAP). RESULTS Fluorescein-dextran angiography delineated the entire vascular pattern, including neovascular tufts in flat-mounted retinas. Hyperoxia-induced neovascularization occurred at the junction between the vascularized and avascular retina in the mid-periphery. Retinal neovascularization occurred in all the pups between postnatal day 17 and postnatal day 21. There was a mean of 89 neovascular nuclei per cross-section of 9 eyes in hyperoxia compared to less than 1 nucleus per cross-section of 8 eyes in the normoxia control (P < 0.0001). Proliferative vessels were not associated with GFAP-positive astrocyte processes. CONCLUSIONS The authors have described a reproducible and quantifiable mouse model of oxygen-induced retinal neovascularization that should prove useful for the study of pathogenesis of retinal neovascularization as well as for the study of medical intervention for ROP and other retinal angiopathies.