Overexpression of mitofusin 2 inhibits reactive astrogliosis proliferation in vitro.

Authors: Liu, Tao  Xue, Chen-chen  Shi, Yu-long  Bai, Xiang-jun  Li, Zhan-fei  Yi, Cheng-la 
Citation: Liu T, etal., Neurosci Lett. 2014 Sep 5;579:24-9. doi: 10.1016/j.neulet.2014.07.002. Epub 2014 Jul 11.
Pubmed: (View Article at PubMed) PMID:25017825
DOI: Full-text: DOI:10.1016/j.neulet.2014.07.002

Astrocytes become activated in response to central nervous system (CNS) injury, and excessive astrogliosis is considered an impediment to axonal regeneration by forming glial scar. Mitofusin 2 (Mfn2), a key protein in mitochondrial network, has been reported to negatively regulate cell proliferation. The present study aimed to explore whether reactive astrogliosis could be suppressed by Mfn2 overexpression. Scratch injury and starvation-serum stimulation models in cultured astrocytes were combined to address this issue. In scratch model, reactive proliferation status of damaged astrocytes was implicated by migration of high ratio of EdU(+) cells into lesion region and significantly increased expression of GFAP and PCNA. At meantime, Mfn2 expression was found to exert a down-regulated trend both in gen and protein levels. Pretreatment of cells with adenoviral vector encoding Mfn2 gene increased Mfn2 expression and subsequently attenuated injury-induced astrocytes hyperplasia, activation-relevant protein synthesis, cellular proliferation, eventually delayed wound healing process. Furthermore, Mfn2 overexpression markedly inhibited astrocytes proliferation induced by serum stimulation, by arresting the transition of cell cycle from G1 to S phase. Together, these in vitro results demonstrated that reactive astrogliosis can be effectively suppressed by up-regulation of Mfn2, which might contribute to a promising therapeutic intervention in CNS disease characterized by glia-related damage.

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CRRD ID: 13204822
Created: 2017-07-20
Species: All species
Last Modified: 2017-07-20
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.