The effects of oxygen stresses on the development of features of severe retinopathy of prematurity: knowledge from the 50/10 OIR model.
The effects of oxygen stresses on the development of features of severe retinopathy of prematurity: knowledge from the 50/10 OIR model.
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DOI：
10.1007/s10633-009-9181-x
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发表时间：
2010-02
影响因子：
1.4
通讯作者：
Hartnett, M. Elizabeth
中科院分区：
文献类型：
--
作者：
Hartnett, M. Elizabeth
关键词：
描述氧波动和补充氧（SO）的影响，与当今早产儿相关的应激，对与玻璃体内新生血管和无血管视网膜相关的生长因子表达和信号通路的激活，以及严重早产儿视网膜病变（ROP）的特征。使用50/10氧诱导视网膜病变（OIR）和50/10 OIR+SO模型的文章综述即使在无血管视网膜持续存在且在玻璃体内新生血管形成之前，氧气的反复波动也会增加视网膜VEGF。缺氧增加VEGF120的表达，而反复波动的氧气增加VEGF164。中和VEGF生物活性显著减少玻璃体内新生血管和小动脉扭曲，而不干扰正在进行的视网膜血管形成。反复的氧波动导致视网膜缺氧和活性氧（ROS）增加。NADPH氧化酶抑制剂罗布麻苷抑制ROS通过干扰细胞凋亡减少无血管视网膜。补充氧气可降低视网膜VEGF浓度，增强NADPH氧化酶的激活，通过激活JAK/STAT通路促进玻璃体内新生血管的形成。与今天早产儿所经历的有关的氧应激触发不同途径的信号，导致视网膜无血管和玻璃体内新生血管。
To describe the effects of oxygen fluctuations and supplemental oxygen (SO), stresses relevant to preterm infants today, on growth factor expression and activation of signaling pathways associated with intravitreous neovascularization and avascular retina, features of severe retinopathy of prematurity (ROP). Review of articles using 50/10 oxygen-induced retinopathy (OIR) and 50/10 OIR+SO models Repeated fluctuations in oxygen increased retinal VEGF even while avascular retina persisted and prior to the development of intravitreous neovascularization. Hypoxia increased VEGF120 expression whereas repeated fluctuations in oxygen increased VEGF164. Neutralizing VEGF bioactivity significantly reduced intravitreous neovascularization and arteriolar tortuosity without interfering with ongoing retinal vascularization. Repeated oxygen fluctuations led to retinal hypoxia and increased reactive oxygen species (ROS). Inhibiting ROS with NADPH oxidase inhibitor, apocynin, reduced avascular retina by interfering with apoptosis. Supplemental oxygen reduced retinal VEGF concentration and exacerbated NADPH oxidase activation to contribute to intravitreous neovascularization through activation of JAK/STAT pathway. Oxygen stresses relevant to those experienced by preterm infants today trigger signaling of different pathways to cause avascular retina and intravitreous neovascularization.
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