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Epithelial membrane protein-2 promotes VEGF signaling to promote pathological neovascular growth in retinopathy of prematurity

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Retinopathy of prematurity (ROP) is a leading cause of childhood blindness, and exclusively affects infants born prematurely. In this study, we test the hypothesis that EMP2 contributes to neovascularization in a mouse model of the disease. We show that EMP2 promotes neuronal VEGF signaling and that its downregulation reduces severity of neovascularization. RNA-Seq was performed on RNA from frozen retinal tissues. Four replicates from the following conditions were profild: WT normoxia, EMP2 KO normoxia, WT hyperoxia, and EMP2 KO hyperoxia group at P17.

早产儿视网膜病变(Retinopathy of prematurity, ROP)是儿童失明的首要致病因素,且仅累及早产新生儿。本研究验证了“EMP2在该疾病的小鼠模型中促进血管新生”这一科学假说。研究证实,EMP2可促进神经元的血管内皮生长因子(Vascular Endothelial Growth Factor, VEGF)信号通路激活,而其表达下调可减轻血管新生的病变严重程度。本研究对冷冻保存的视网膜组织提取的总RNA开展了RNA测序(RNA-Seq)。在出生后第17天(P17),针对下述四组实验条件各设置4次生物学重复并完成了转录组表达谱分析:野生型(Wild Type, WT)常氧组、EMP2敲除(Knockout, KO)常氧组、野生型高氧组、EMP2敲除高氧组。

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