Repetitive Transcranial Magnetic Stimulation Alleviates Neurological Deficits After Cerebral Ischemia Through Interaction Between RACK1 andBDNF exon IVby the Phosphorylation-Dependent Factor MeCP2

Repetitive Transcranial Magnetic Stimulation Alleviates Neurological Deficits After Cerebral Ischemia Through Interaction Between RACK1 andBDNF exon IVby the Phosphorylation-Dependent Factor MeCP2
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重复经颅磁刺激通过磷酸化依赖因子MeCP 2与RACK 1和BDNF外显子IV的相互作用减轻脑缺血后的神经功能缺损

DOI:
10.1007/s13311-019-00771-y
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发表时间:
2020-04-01
期刊:
影响因子:
5.7
通讯作者:
Zhou, Xianju
Zhou, Xianju
中科院分区:
医学2区
文献类型:
--
作者:
Li, Hongzhan;Shang, Jianqing;Zhou, Xianju

文献摘要

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Repetitive transcranial magnetic stimulation (rTMS) is acknowledged as a form of neurostimulation, especially for functional recovery. The foundational knowledge of molecular mechanism is limited regarding its role in cerebral ischemia, for which the present study was designed. Primary neurons were treated with oxygen-glucose deprivation (OGD) and repetitive magnetic stimulation (rMS), in which brain-derived neurotrophic factor (BDNF) and transcription ofBDNF exonswere examined. Then, adenovirus vectors carrying siRACK1 sequence were delivered to primary neurons, followed by detection of the transcription ofBDNF exonsand the extent of methyl CpG binding protein 2 (MeCP2) phosphorylation. Results showed that BDNF and the transcription ofBDNF exonswere upregulated by rMS and OGD treatment, but decreased by extra treatment of RACK1 siRNA. Then, the mechanism investigations demonstrated that rMS increased the extent of MeCP2 phosphorylation to promote the interaction between RACK1 andBDNF exon IV. The aforementioned findings were further confirmedin vivoin middle cerebral artery occlusion (MCAO)-induced rat models, as indicated by improved neurological functions and reduced area of cerebral infarction. The study offers potential evidence for improvement of neurological deficits, highlighting the important role of rTMS for treatment of cerebral ischemia.