Journal of integrative neuroscience · 2025
Electroacupuncture Regulates Mitochondria-Endoplasmic Reticulum interactions via Fn1 in a Parkinson's Disease Model: Transcriptomic Evidence.
СтатьяНазвание и аннотация: Перевод в очереди
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Lyu Peilin, Wen Feng, Fu Zhiyi, Li Junying, Li Qiyan, Cai Xiaowen, Huang Shengtao, Qiu Xiaoke, Zhang Zhinan, Huang Yong, Zhang Jiping
Аннотация
AIMS: Parkinson's disease (PD) is characterized by dopaminergic neuron degeneration and disruption to mitochondria-associated endoplasmic reticulum membranes (MAMs). This study explores whether electroacupuncture (EA) can alleviate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced PD symptoms and investigates the underlying mechanisms using RNA sequencing (RNA-seq).
METHODS: A PD mouse model was established using MPTP, followed by EA treatment at governing vessel 20 (GV20) and gallbladder meridian 34 (GB34) acupoints, with sham EA treatments as a control. Behavioral assays, immunohistochemistry, and Western blotting assessed neuroprotective effects. MAM integrity was assessed using Western blot, immunofluorescence staining, and transmission electron microscopy. RNA-seq and protein-protein interaction (PPI) analysis identified differentially expressed genes which were validated by real-time fluorescence quantitative polymerase chain reaction (qRT-PCR).
RESULTS: EA treatment improved motor performance, increased substantia nigra (SN) and striatum tyrosine hydroxylase expression, reduced SN alpha-synuclein, and improved SN dopamine neuron MAM structure. Transcriptomic analysis identified 32 MAM-associated genes, of which fibronectin-1 (Fn1) was identified as a key regulator. EA was found to upregulate Fn1 expression, suggesting its involvement in MAM stabilization and neuroprotection.
CONCLUSION: EA at GV20 and GB34 alleviated motor and neural impairments in a PD mouse model potentially through modulation of Fn1 and its role in MAM-associated pathways.
METHODS: A PD mouse model was established using MPTP, followed by EA treatment at governing vessel 20 (GV20) and gallbladder meridian 34 (GB34) acupoints, with sham EA treatments as a control. Behavioral assays, immunohistochemistry, and Western blotting assessed neuroprotective effects. MAM integrity was assessed using Western blot, immunofluorescence staining, and transmission electron microscopy. RNA-seq and protein-protein interaction (PPI) analysis identified differentially expressed genes which were validated by real-time fluorescence quantitative polymerase chain reaction (qRT-PCR).
RESULTS: EA treatment improved motor performance, increased substantia nigra (SN) and striatum tyrosine hydroxylase expression, reduced SN alpha-synuclein, and improved SN dopamine neuron MAM structure. Transcriptomic analysis identified 32 MAM-associated genes, of which fibronectin-1 (Fn1) was identified as a key regulator. EA was found to upregulate Fn1 expression, suggesting its involvement in MAM stabilization and neuroprotection.
CONCLUSION: EA at GV20 and GB34 alleviated motor and neural impairments in a PD mouse model potentially through modulation of Fn1 and its role in MAM-associated pathways.