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Electroacupuncture Restores Locomotor Functions After Mouse Spinal Cord Injury in Correlation With Reduction of PTEN and p53 Expression
被引:15
作者:
Wei, Zhe
[1
,2
]
Zhao, Weijiang
[1
]
Schachner, Melitta
[1
,3
]
机构:
[1] Shantou Univ, Med Coll, Ctr Neurosci, Shantou, Peoples R China
[2] Lishui Univ, Fac Med & Hlth, Lishui, Peoples R China
[3] Rutgers State Univ, Dept Cell Biol & Neurosci, Piscataway, NJ USA
基金:
中国国家自然科学基金;
关键词:
electroacupuncture;
spinal cord injury;
p53;
PTEN;
mTOR;
mouse;
CELL-ADHESION MOLECULE;
CATENIN SIGNALING PATHWAY;
NEURAL STEM-CELLS;
IMMUNOGLOBULIN SUPERFAMILY;
INDUCED APOPTOSIS;
RECOVERY;
PROMOTES;
RATS;
L1;
PROLIFERATION;
D O I:
10.3389/fnmol.2018.00411
中图分类号:
Q189 [神经科学];
学科分类号:
071006 [神经生物学];
摘要:
Background: We previously showed that electroacupuncture (EA) at Jiaji points promotes expression of adhesion molecule L1 in spinal cord tissue after mouse spinal cord injury (SCI) and contributes to recovery of neural functions. Objective: We investigated the effects of EA on downstream signaling molecules of L1 and molecules relevant to apoptosis with the aim to understand the underlying molecular mechanisms. Methods: Female C57BL/6 mice were divided into a sham group, injury group, injury+acupuncture (AP) group and injury+EA group. We investigated the changes in cognate L1-triggered signaling molecules after SCI by immunofluorescence staining and immunoblot analysis. Results: Protein levels of phosphatase and tensin homolog (PTEN) and p53 were decreased by EA at different time points after injury, whereas the levels of phosphorylated mammalian target of rapamycin (pmTOR), p-Akt and phosphorylated extracellular signal-regulated kinase (p-Erk) were increased. Also, levels of myelin basic protein (MBP) were increased by EA. AP alone showed less pronounced changes in expression of the investigated molecules, when compared to EA. Conclusion: We propose that EA contributes to neuroprotection by inhibiting PTEN and p53 expression and by increasing the levels of pmTOR/Akt/Erk and of MBP after SCI. These observations allow novel insights into the beneficial effects of EA via L1-triggered signaling molecules after injury.
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页数:12
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