Budd Steven J, Thompson Hilary, Hartnett M Elizabeth
Department of Ophthalmology, University of North Carolina, Chapel Hill, USA.
Arch Ophthalmol. 2010 Aug;128(8):1014-21. doi: 10.1001/archophthalmol.2010.158.
To study the effects of oxygen fluctuations on rat vascular endothelial growth factor (VEGF), VEGF receptor 1(VEGFR1), and VEGFR2 in a model of retinopathy of prematurity (ROP).
Retinas at several postnatal days (p) were analyzed for VEGF splice variants, VEGFR1 and VEGFR2 messenger RNAs (mRNAs) using real-time polymerase chain reaction or for VEGF protein using enzyme-linked immunosorbent assay.
Older developmental age was associated with VEGFR1 (P < .001), VEGF(120) (P < .001), and VEGF(188) (P = .03) mRNA overexpression. Expression of VEGFR2 and VEGF(164) mRNAs were associated with older age (P < .001) or exposure to the ROP model (P = .02 and P < .001, respectively). Expression of VEGF protein was greater at p14, when 30% avascular retina existed in the ROP model, compared with room air, when no avascular retina existed, and at p18, when intravitreous neovascularization existed in the model but not in room air (P < .001 for both).
Unlike models of oxygen-induced retinopathy that describe ROP before implementation of oxygen regulation, the ROP model re-creates oxygen stresses relevant to preterm infants with severe ROP today. Expression of VEGF(164) and VEGFR2 mRNAs and VEGF protein were increased in association with the ROP model and older developmental age and at time points when not only intravitreous neovascularization but also avascular retina were present in the ROP model and not in room air. Clinical Relevance Regulation of VEGF may have a role in the development of avascular retina and intravitreous neovascularization in some forms of severe ROP.
在早产儿视网膜病变(ROP)模型中研究氧波动对大鼠血管内皮生长因子(VEGF)、VEGF受体1(VEGFR1)和VEGFR2的影响。
使用实时聚合酶链反应分析出生后几天(p)视网膜中的VEGF剪接变体、VEGFR1和VEGFR2信使核糖核酸(mRNA),或使用酶联免疫吸附测定法分析VEGF蛋白。
发育年龄较大与VEGFR1(P <.001)、VEGF(120)(P <.001)和VEGF(188)(P =.03)mRNA过表达相关。VEGFR2和VEGF(164) mRNA的表达与年龄较大(P <.001)或暴露于ROP模型相关(分别为P =.02和P <.001)。与不存在无血管视网膜的室内空气相比,在ROP模型中存在30%无血管视网膜的p14时,VEGF蛋白表达更高;与室内空气相比,在模型中存在玻璃体内新生血管而室内空气不存在的p18时,VEGF蛋白表达更高(两者P均 <.001)。
与在实施氧调节之前描述ROP的氧诱导视网膜病变模型不同,ROP模型再现了与当今患有严重ROP的早产儿相关的氧应激。VEGF(164)和VEGFR2 mRNA以及VEGF蛋白的表达与ROP模型、发育年龄较大以及ROP模型中存在玻璃体内新生血管和无血管视网膜而室内空气不存在的时间点相关。临床意义VEGF的调节可能在某些形式的严重ROP中无血管视网膜和玻璃体内新生血管的发展中起作用。