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Knockdown of PDCD4 ameliorates neural cell apoptosis and mitochondrial injury through activating the PI3K/AKT/mTOR signal in Parkinson's disease

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机构： [1]Department of Neurology, The First Hospital of Hebei Medical University, Shijiangzhuang, Hebei 050031, China [2]Department of Neurology, Hebei Hospital of Xuanwu Hospital Capital Medical University, Shijiazhuang, Hebei, 050031, China [3]Department of Respiratory Medicine, Harrison International Peace Hospital, Hengshui, Hebei 053000, China

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关键词： Parkinson’s disease PDCD4 Apoptosis Mitochondrial injury PI3K/AKT/mTOR signal

摘要：

Parkinson's disease (PD) is a complex neurodegenerative disorder and hampers normal living. It has been reported that programmed cell death 4 (PDCD4) is associated with tumor suppression, inflammatory response, and apoptosis.The aim of this study was to investigate the role of PDCD4 in PD.The in vivo and in vitro PD models were established by MPTP-induced mice and MMP+ stimulated MN9D cells, respectively. The expression of PDCD4 was detected by western blot. The MN9D cell viability and apoptosis were determined by MTT and flow cytometry assay. Moreover, the MN9D cell mitochondrial injury was evaluated by JC-1 staining.In this study, PDCD4 was highly expressed in brain tissue of MPTP-induced PD mouse model. In a loss-function experiments, knockdown of PDCD4 promoted MN9D cell viability and allayed MPP+-triggered MN9D cell apoptosis. Furthermore, knockdown of PDCD4 ameliorated MPP+-evoked MN9D cell mitochondrial injury. Mechanically, knockdown of PDCD4 abolished the effect of MMP+ stimulation via activating phosphoinositide 3-kinase(PI3K)/AKT/mammalian target of rapamycin (mTOR) signal. Notably, the protective effects of shPDCD4 on cell apoptosis and mitochondrial injury were suppressed by PI3K inhibitor LY294002.In summary,knockdown of PDCD4 ameliorates neural cell apoptosis and mitochondrial injury through activating the PI3K/AKT/mTOR signal, providing a novel target for PD treatment.All data generated or analyzed during this study are included in this published article.Copyright © 2023 Elsevier B.V. All rights reserved.

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出版当年[2022]版：

大类 | 4 区医学

小类 | 4 区生化与分子生物学 4 区神经科学

最新[2023]版：

大类 | 4 区医学

小类 | 4 区生化与分子生物学 4 区神经科学

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出版当年[2021]版：

Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Q3 NEUROSCIENCES

最新[2023]版：

Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Q3 NEUROSCIENCES

影响因子： 2.7 最新[2023版] 2.6 最新五年平均 3.097 出版当年[2021版] 3.019 出版当年五年平均 3.052 出版前一年[2020版] 2.8 出版后一年[2022版]

第一作者：

第一作者机构： [1]Department of Neurology, The First Hospital of Hebei Medical University, Shijiangzhuang, Hebei 050031, China [2]Department of Neurology, Hebei Hospital of Xuanwu Hospital Capital Medical University, Shijiazhuang, Hebei, 050031, China [*1]Department of Neurology, The First Hospital of Hebei Medical University, No. 89 Donggang Road, Yuhua District, Shijiazhuang, Hebei, China.

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通讯作者：

通讯机构： [1]Department of Neurology, The First Hospital of Hebei Medical University, Shijiangzhuang, Hebei 050031, China [2]Department of Neurology, Hebei Hospital of Xuanwu Hospital Capital Medical University, Shijiazhuang, Hebei, 050031, China [*1]Department of Neurology, The First Hospital of Hebei Medical University, No. 89 Donggang Road, Yuhua District, Shijiazhuang, Hebei, China.

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Knockdown of PDCD4 ameliorates neural cell apoptosis and mitochondrial injury through activating the PI3K/AKT/mTOR signal in Parkinson's disease

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