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Neuroprotective Effects of Transcription Factor Brn3b in an Ocular Hypertension Rat Model of Glaucoma

机译:转录因子Brn3b在青光眼高眼压大鼠模型中的神经保护作用

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摘要

Purpose.Glaucoma is an optic neuropathy commonly associated with elevated intraocular pressure (IOP), leading to optic nerve head (ONH) cupping, axon loss, and apoptosis of retinal ganglion cells (RGCs), which could ultimately result in blindness. Brn3b is a class-4 POU domain transcription factor that plays a key role in RGC development, axon outgrowth, and pathfinding. Previous studies suggest that a decrease in Brn3b levels occurs in animal models of glaucoma. The goal of this study was to determine if adeno-associated virus (AAV)-directed overexpression of the Brn3b protein could have neuroprotective effects following elevated IOP-mediated neurodegeneration.
机译:目的青光眼是一种视神经病变,通常与眼内压(IOP)升高有关,导致视神经头(ONH)拔罐,轴突丢失和视网膜神经节细胞(RGC)凋亡,最终可能导致失明。 Brn3b是4类POU结构域转录因子,在RGC发育,轴突生长和寻路中起关键作用。先前的研究表明,在青光眼的动物模型中Brn3b水平降低。这项研究的目的是确定在IOP介导的神经变性升高后,腺相关病毒(AAV)指导的Brn3b蛋白过度表达是否具有神经保护作用。

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