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Dab2 attenuates brain injury in APP/PS1 mice via targeting transforming growth factor-beta/SMAD signaling 被引量:4
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作者 Lei Song Yue Gu +4 位作者 Jing Jie xiaoxue bai Ying Yang Chaoying Liu Qun Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第1期41-50,共10页
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 aggr... 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 T RII from degradation and ensures the effective conduction of TGF-β 1/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 signifi- cantly increased, while amyloid-beta deposition, microglia activation, tumor necrosis factor- and 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. 展开更多
关键词 nerve regeneration transforming growth factor-β1 Dab2 Alzheimer's disease amyol-id-beta NEURON SMAD2 SMAD3 MICROGLIA neural regeneration
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