Dab2 attenuates brain injury in APP/PS1 mice via targeting transforming growth factor-beta/SMAD signaling

查看全文 作　　者：Lei [1]Song;Yue [2]Gu;Jing [2]Jie;Xiaoxue [2]Bai;Ying [2]Yang;Chaoying [2]Liu;Qun [1]Liu

机构地区：[1]Department of Neurology,Norman Bethune First Hospital of Jilin University;[2]Department of Respiratory Medicine,Norman Bethune First Hospital of Jilin University

出　　处：《Neural Regeneration Research》索引2014年第9卷第1期,共10页

摘　　要：Transforming growth factor-beta(TGF-β)type II receptor(TβRII)levels are extremely low in the brain tissue of patients with Alzheimer’s disease.This receptor inhibits TGF-β1/SMAD signaling and thereby aggravates amyolid-beta deposition and neuronal injury.Dab2,a specific adapter protein,protects TβRII from degradation and ensures the effective conduction of TGF-β1/SMAD signaling.In this study,we used an adenoviral vector to overexpress the Dab2 gene in the mouse hippocampus and investigated the regulatory effect of Dab2 protein on TGF-β1/SMAD signaling in a mouse model of Alzheimer’s disease,and the potential neuroprotective effect.The results showed that the TβRII level was lower in APP/PS1 mouse hippocampus than in normal mouse hippocampus.After Dab2 expression,hippocampal TβRII and p-SMAD2/3 levels were significantly increased,while amyloid-beta deposition,microglia activation,tumor necrosis factor-βand interleulin-6 levels and neuronal loss were significantly attenuated in APP/PS1 mouse brain tissue.These results suggest that Dab2 can exhibit neuroprotective effects in Alzheimer’s disease by regulating TGF-β1/SMAD signaling. 关键词：转化生长因子-Β 小鼠模型信号衰减阿尔茨海默氏病脑损伤神经保护作用 TGF-β 肿瘤坏死因子-α

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Dab2 attenuates brain injury in APP/PS1 mice via targeting transforming growth factor-beta/SMAD signaling

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