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TRA2A-induced upregulation of LINC00662 regulates blood-brain barrier permeability by affecting ELK4 mRNA stability in Alzheimer's microenvironment

biorxiv. 2019; 
Qianshuo Liu,  Lu Zhu,  Xiaobai Liu,  Jian Zheng,  Yunhui Liu,  Xuelei Ruan,  Shuo Cao,  Heng Cai,  Zhen Li,  
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Gene Synthesis Silencing plasmid of LINC00662 was ligated into LV10 (U6/RFP&Puro) vector (GenePharma, Shanghai, China) to construct the shLINC00662 plasmid. Short-hairpin RNA directed against human TRA2A gene, STAU1 gene, UPF1 gene and ELK4 gene was ligated into the pGPU6/GFP/Neo vector (GenePharma) to construct shTRA2A, shSTAU1, shUPF1, and shELK4 plasmid, respectively. The human ELK4 gene coding sequence was ligated into pIRES2 vector (GenScript, Piscataway, NJ, USA) to construct the ELK4 overexpression plasmid. Get A Quote

摘要

The blood-brain barrier (BBB) has an important significance in maintenance and regulation of the neural microenvironment. The occurrence of BBB disruption is the pathological change of early Alzheimer’s disease (AD). RNA-binding proteins and long non-coding RNAs are closely related to the regulation of BBB permeability. Our study was performed to demonstrate TRA2A/LINC00662/ELK4 axis that regulates BBB permeability in AD microenvironment. In Aβ1-42-incubated microvascular endothelial cells (ECs) of BBB model in vitro, TRA2A and LINC00662 were enriched. TRA2A increased the stability of LINC00662 by binding with it. The knockdown of either TRA2A or LINC00662 decreased the BBB permeability via upregulating t... More

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