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Changes in components of the neurovascular unit in the retina in a rat model of retinopathy of prematurity

机译:Retina在早熟视网膜病变大鼠视网膜中神经血管单元组分的变化

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摘要

An impairment of cellular interactions between the elements of the neurovascular unit contributes to the onset and/or progression of retinal diseases. The present study aims to examine how elements of the neurovascular unit are altered in a rat model of retinopathy of prematurity (ROP). Neonatal rats were treated subcutaneously with the vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor KRN633 (10 mg/kg) on postnatal day (P) 7 and P8 to induce ROP. Morphological assessments were performed of blood vessels, astrocytes and neuronal cells in the retina. Aggressive angiogenesis, tortuous arteries and enlarged veins were observed in the retinal vasculature of KRN633-treated (ROP) rats from P14 to P28, compared to age-matched control (vehicle-treated) animals. Morphological abnormalities in the retinal vasculature showed a tendency toward spontaneous recovery from P28 to P35 in ROP rats. Immunofluorescence staining for glial fibrillary acidic protein and Pax2 (astrocyte markers) revealed that morphological changes to and a reduction in the number of astrocytes occurred in ROP rats. The developmental cell death was slightly accelerated in ROP rats; however, no visible changes in the morphology of retinal layers were observed on P35. The abnormalities in astrocytes might contribute, at least in part, to the formation of abnormal retinal blood vessels and the pathogenesis of ROP.
机译:神经血管单元的元素之间的细胞相互作用有助于视网膜疾病的发病和/或进展。本研究旨在检测神经血管单元的元素如何在早产儿(ROP)视网膜病变的大鼠模型中改变。在后期(P)7和P8上,用血管内皮生长因子(VEGF)受体酪氨酸激酶抑制剂KRN633(10mg / kg)皮下治疗新生大鼠,以诱导ROP。对视网膜中的血管,星形胶质细胞和神经元细胞进行形态学评估。与A年龄匹配的对照(载体处理)的动物相比,在P14至P28的Krn633处理(ROP)大鼠的视网膜脉管系统中观察到侵袭性血管生成,曲折的动脉和扩大静脉。视网膜脉管系统的形态异常表现出从罗珀大鼠P28到P35的自发恢复的趋势。用于胶质纤维酸性蛋白和PAX2(星形胶质细胞标志物)的免疫荧光染色表明,在ROP大鼠中发生的形态变化和半胶质细胞数量的减少。 ROP大鼠的发育细胞死亡略微加速;然而,在P35上观察到视网膜层的形态的可见变化。星形胶质细胞的异常至少部分地促进形成异常的视网膜血管和ROP的发病机制。

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