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Neuroprotective Effect of A20 on TNF-Induced Postischemic Apoptosis

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An Erratum to this article was published on 29 September 2006

Focal cerebral ischemia causes apoptosis in neural cells during the postischemia period. TNF is critically involved in such neuronal apoptosis mediated by caspase pathways. A20 can inhibit TNF-induced apoptosis in many cell types. However, little work has been carried out in central nervous system. In the present study, gene transfer of A20 resulted in reduction of infarct volume and improvement of neurological deficit in ischemia rats. Results of flow cytometry, TUNEL and DNA fragmentation assay all indicated A20 could inhibit TNF-induced apoptosis both in primary rat hippocampal neurons and SH-SY5Y cells. Moreover, we found A20 targeted the TNF apoptotic pathway by inhibiting proteolytic cleavage of caspase 8 and 3 in SH-SY5Y cells. These data demonstrated A20 could effectively protect neurons from postischemic apoptosis and may function partly on death receptor caspase pathway. Gene transfer of A20 may be a promising approach to gene therapy for cerebral ischemia in the future.

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Authors and Affiliations

  1. Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Room 901, Cell Biology Building, No. 320 Yueyang Road, Shanghai, 200031, China

    Luyang Yu, Hongsheng Miao, Yanan Hou, Bao Zhang & Lihe Guo

  2. Graduate School of the Chinese Academy of Sciences, China

    Luyang Yu, Yanan Hou & Bao Zhang

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  1. Luyang Yu
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  2. Hongsheng Miao
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Correspondence to Lihe Guo.

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Luyang Yu and Hongsheng Miao - These two authors contribute equally to this work

An erratum to this article is available at http://dx.doi.org/10.1007/s11064-006-9163-2.

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Yu, L., Miao, H., Hou, Y. et al. Neuroprotective Effect of A20 on TNF-Induced Postischemic Apoptosis. Neurochem Res 31, 21–32 (2006). https://doi.org/10.1007/s11064-005-9004-8

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