Affiliation(s):
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, China;
moreAffiliation(s): Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, China; Xi’an Center for Disease Control and Prevention, Xi’an 710000, China; NHC Key Laboratory of Etiology and Epidemiology (Harbin Medical University), Harbin 150081, China; Joint Key Laboratory of Endemic Diseases (Harbin Medical University, Guizhou Medical University, Xi’an Jiaotong University), Harbin 150081, China;
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Xinbo MA, Liu YANG, Xinhua SHAO, Jia CUI, Ziqiao GUAN, Man LV, Shuaifei YANG, Na FANG, Yang LIU, Yanhui GAO, Xiaona LIU, Yanmei YANG. Reduced NGF mediates arsenic-induced mitochondrial dynamic imbalance and neuronal damage both in vivo and in vitro[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B2500216
@article{title="Reduced NGF mediates arsenic-induced mitochondrial dynamic imbalance and neuronal damage both in vivo and in vitro", author="Xinbo MA, Liu YANG, Xinhua SHAO, Jia CUI, Ziqiao GUAN, Man LV, Shuaifei YANG, Na FANG, Yang LIU, Yanhui GAO, Xiaona LIU, Yanmei YANG", journal="Journal of Zhejiang University Science B", year="in press", publisher="Zhejiang University Press & Springer", doi="https://doi.org/10.1631/jzus.B2500216" }
%0 Journal Article %T Reduced NGF mediates arsenic-induced mitochondrial dynamic imbalance and neuronal damage both in vivo and in vitro %A Xinbo MA %A Liu YANG %A Xinhua SHAO %A Jia CUI %A Ziqiao GUAN %A Man LV %A Shuaifei YANG %A Na FANG %A Yang LIU %A Yanhui GAO %A Xiaona LIU %A Yanmei YANG %J Journal of Zhejiang University SCIENCE B %P %@ 1673-1581 %D in press %I Zhejiang University Press & Springer doi="https://doi.org/10.1631/jzus.B2500216"
TY - JOUR T1 - Reduced NGF mediates arsenic-induced mitochondrial dynamic imbalance and neuronal damage both in vivo and in vitro A1 - Xinbo MA A1 - Liu YANG A1 - Xinhua SHAO A1 - Jia CUI A1 - Ziqiao GUAN A1 - Man LV A1 - Shuaifei YANG A1 - Na FANG A1 - Yang LIU A1 - Yanhui GAO A1 - Xiaona LIU A1 - Yanmei YANG J0 - Journal of Zhejiang University Science B SP - EP - %@ 1673-1581 Y1 - in press PB - Zhejiang University Press & Springer ER - doi="https://doi.org/10.1631/jzus.B2500216"
Abstract: Arsenic exposure is known to cause cognitive deficits, although the underlying mechanisms are yet to be explored. In this study, we investigated the role of nerve growth factor (NGF), a neuroprotective factor, in arsenic-induced cognitive impairment. In mouse models exposed to 25 mg/L and 50 mg/L sodium arsenite (NaAsO2), we observed neuronal damage accompanied by the downregulation of NGF, decreased phosphorylation of phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT), reduced phosphorylation of the mitochondrial fission protein dynamin-related protein 1 (Drp1), and downregulation of the mitochondrial fusion protein optic atrophy 1 (OPA1). Similarly, the downregulation of NGF, inactivation of the PI3K/AKT signaling pathway, mitochondrial dynamics imbalance (dysregulation of mitochondrial fission and fusion processes), and increased apoptosis were observed in HT-22 cells exposed to 4 μmol/L NaAsO2. NGF overexpression mitigated these arsenic-induced alterations, while the protective effect of NGF against arsenic toxicity was reduced by LY294002, a PI3K/AKT pathway inhibitor. These findings suggest that a decrease in NGF mediates the arsenic-disrupted mitochondrial dynamics via inhibiting the PI3K/AKT pathway, ultimately impairing cognitive function.
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