Electrical stimulation enhances neurogenin2 expression through β-catenin signaling pathway of mouse bone marrow stromal cells and intensifies the effect of cell transplantation on brain injury

IF 2 4区 医学 Q3 NEUROSCIENCES Neuroscience Letters Pub Date : 2013-01-15 DOI:10.1016/j.neulet.2012.10.023
Masaya Matsumoto , Takeshi Imura , Takahiro Fukazawa , Yanan Sun , Masaaki Takeda , Teruyuki Kajiume , Yumi Kawahara , Louis Yuge
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引用次数: 22

Abstract

Bone marrow stromal cells (BMSCs) have received significant attention for its use in neural regeneration. However, neural replacement by transplanted BMSCs was not very effective. Recently, the gene transfection method has improved the capability of cell transplantation; however, this method results in canceration and immune rejection. We induced the differentiation of mouse BMSCs into neural cells using electrical stimulation and transplanted the cells into traumatic brain injury (TBI) model mice. We found that the electrically stimulated cells have good potential to differentiate into neural cells and contribute to recovery from TBI without differentiating into astrocytes. In addition, we found that electrical stimulation enhanced neurogenin2 (Ngn2) expression. Ngn2 is involved in neural differentiation and inhibits astrocytic differentiation during cell growth. Furthermore, we found that this enhancement of Ngn2 expression occurred through β-catenin signaling pathway. This study may contribute to the use of BMSCs for neural replacement in central nervous system diseases.

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电刺激通过小鼠骨髓基质细胞β-catenin信号通路增强neurogenin2的表达,增强细胞移植对脑损伤的影响
骨髓基质细胞(BMSCs)因其在神经再生中的应用而受到广泛关注。然而,移植骨髓间充质干细胞的神经替代效果不佳。近年来,基因转染方法提高了细胞移植的能力;然而,这种方法会导致癌变和免疫排斥。利用电刺激诱导小鼠骨髓间充质干细胞向神经细胞分化,并将其移植到创伤性脑损伤(TBI)模型小鼠体内。我们发现,电刺激的细胞有很好的潜力分化为神经细胞,有助于从TBI恢复而不分化为星形胶质细胞。此外,我们发现电刺激增强了神经原蛋白2 (Ngn2)的表达。Ngn2参与神经分化,并在细胞生长过程中抑制星形细胞分化。此外,我们发现这种Ngn2表达的增强是通过β-catenin信号通路发生的。本研究可能有助于骨髓间充质干细胞用于中枢神经系统疾病的神经替代。
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来源期刊
Neuroscience Letters
Neuroscience Letters 医学-神经科学
CiteScore
5.20
自引率
0.00%
发文量
408
审稿时长
50 days
期刊介绍: Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.
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