Proteomes analysis reveals the involvement of autophagy in AD-like neuropathology induced by noise exposure and ApoE4

神经病理学 生物 PI3K/AKT/mTOR通路 蛋白质组 蛋白质组学 神经科学 海马体 凝集素 神经颗粒素 神经退行性变 神经发生 载脂蛋白E 细胞生物学 信号转导 生物信息学 医学 基因 遗传学 疾病 病理 细胞凋亡 蛋白激酶C
作者
Wenlong Li,Donghong Su,Qingfeng Zhai,Huimin Chi,Xiaojun She,Xiujie Gao,Kun Wang,Honglian Yang,Rui Wang,Bo Cui
出处
期刊:Environmental Research [Elsevier]
卷期号:176: 108537-108537 被引量:15
标识
DOI:10.1016/j.envres.2019.108537
摘要

Noise is one of the most important environmental health hazards for humans. Environmental noise or apolipoprotein ε4 (ApoE4) can cause typical Alzheimer's disease (AD)-like pathological changes, which is characterized by progressive cognitive decline and neurodegenerative lesions. Gene-environment interactions may accelerate cognitive decline and increase AD risk. However, there is limited experimental evidence regarding the underlying mechanisms of noise-ApoE4 interactions and AD, which may be closely related to AD development.In this study, we investigated the combined effects of chronic noise exposure and the ApoE4 gene activation on hippocampus by using proteomics and differentially expressed proteins were found through performed gene ontology function and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. In addition, we assessed the changes in adult hippocampal neurogenesis and potential underlying mechanism for AD-like neuropathology.Relative to control rats, combined exposure of noise and ApoE4 synergistically increased the characteristic pathological amyloid β-protein of AD-like neuropathology changes in hippocampus. The research identifies a total of 4147 proteins and 15 differentially expressed proteins in hippocampus. Furthermore, comparison of several of the diverse key pathways studied (e.g., PI3K/AKT, insulin, calpain-CDK5, and mammalian target of rapamycin (mTOR) signaling pathways) help to articulate the different mechanisms involved in combined effects of noise and ApoE4 on AD-like pathology. We verified four selected proteins, namely, eukaryotic translation elongation factor 1 epsilon 1, glycine amidinotransferase, nucleoredoxin, and tuberous sclerosis 1 proteins. Validation data shows significant effects of chronic noise and ApoE4 on the expression of four selected proteins, eukaryotic translation elongation factor 1 epsilon 1, glycine amidinotransferase, nucleoredoxin, and tuberous sclerosis 1 proteins, and mTOR and autophagy-related proteins, which share significant interaction effect of chronic noise and ApoE4.Gene-environment interactions between chronic noise and ApoE4 activate the mTOR signaling, decrease autophagy, and facilitate AD-like changes in the hippocampus. Thus, our findings may help elucidate the role of gene-environment interactions in AD development.
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