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SVCT2 Promotes Neural Stem/Progenitor Cells Migration Through
AAV and LV transduction SVCT2 were used for overexpression or SVCT2 interference in vivo and in vitro. (All viruses were packaged by BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Control  rAAV-Ef1a-pA
Custom-Made AAVs  rAAV-Ef1a-SVCT2-pA
 rAAV-U6-shRNA(SVCT2)-Ef1a-pA
LV  rLV-CMV-pA
 rLV-Ef1a-SVCT2-pA
 rLV-U6-shRNA(SVCT2)-pA
Pub Date: 2019-09-19,DOI: 10.3389/fncel.2019.00429,  Email: [email protected]
Yang Yang, Kaiyuan Zhang, Xuezhu Chen, Ju Wang, Xuejiao Lei, Jun Zhong, Jishu Xian, Yulian Quan, Yongling Lu, Qianying Huang, Jingyu Chen, Hongfei Ge and Hua Feng
Ischemic stroke is one of the most leading diseases causing death/long-term disability worldwide. Activating endogenous neural stem/progenitors cells (NSPCs), lining in the subventricular zone (SVZ) and dentate gyrus, facilitates injured brain tissue recovery in both short and long-term experimental settings. While, only a few proliferated NSPCs migrate toward the lesions to enhance endogenous repair after ischemia. Here, the results indicated that the functional recovery was evidently improved and the infarct volume was significantly reduced with ascorbic acid (AA) treatment in a dose-dependent manner from 125 to 500 mg/Kg, and the suitable therapeutic concentration was 250 mg/Kg. The possible mechanism might be due to activating sodium-vitamin C cotransporter 2 (SVCT2), which was down-regulated in SVZ after ischemia. Furthermore, immunostaining images depicted the number of migrated NSPCs from SVZ were significantly increased with 250 mg/Kg AA treatment or SVCT2 overexpression under the physiological and pathological condition in vivo. Besides, the data also represented that 250 mg/Kg AA or SVCT2 overexpression facilitated NSPCs migration via promoting F-actin assembling in the manner of up-regulating CDC42 expression using oxygen-glucose deprivation in vitro. Collectively, the present study indicates that SVCT2 promotes NSPCs migration through CDC42 activation to facilitate F-actin assembling, which enlarges the therapeutic scope of AA and the role of SVCT2 in NSPCs migration after brain injury.
 
Fig1. VCT2 over-expression facilitates NSPCs migration in vivo.
To identify the role of SVCT2 in potentiating endogenous NSPCs migration, using AAV and LV (From BrainVTA) for SVCT2 gene overexpression or interference in this study, the data indicated that SVCT2 promotes NSPCs migration through CDC42 activation to facilitate F-actin assembling, which enlarges the therapeutic scope of AA and the role of SVCT2 in NSPCs migration after brain injury.

BrainVTA offers viral vector construction & virus packaging services for AAV, LV, RABV, PRV, HSV and VSV that help researchers explore questions about genes, neurons, circuitry structure, function of brain network, mechanism and treatment of diseases.
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