GADD34 gene restores virulence in viral vector used in experimental stroke study
GADD34 gene restores virulence in viral vector used in experimental stroke study
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DOI：
10.1038/sj.jcbfm.9600565
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发表时间：
2008-04-01
影响因子：
6.3
通讯作者：
Macrae, I. Mhairi
中科院分区：
文献类型：
--
作者：
McCabe, Christopher;White, Fiona;Macrae, I. Mhairi
GADD 34在缺血性脑中表达并逆转蛋白质合成关闭。因此，GADD 34可能在中风中具有神经保护潜力。BHK培养基是一种复制缺陷型HSV病毒载体（HSV 1716），无插入片段或含有全长GADD 34、N端或基因保守部分，在中风前注射到小鼠脑中。CT大小分别为1.0 +/- 0.26、1.19 +/- 0.36、1.5 +/- 0.36、1.3 +/- 0.36和1.1 +/- 0.28 mm（3）。全长GADD 34的梗死面积增加具有统计学显著性（P < 0.05）。免疫组化证实病毒蛋白表达。组织培养研究显示GADD 34基因在HSV 1716中恢复了毒力，表明HSV毒力而不是增加GADD 34加剧了缺血性损伤。
GADD34 is expressed in the ischaemic brain and reverses protein synthesis shutdown. Consequently, GADD34 could have neuroprotective potential in stroke. BHK medium, a replication-deficient HSV viral vector (HSV1716) with no insert or containing full-length GADD34, the N terminal or a conserved portion of the gene, was injected into mouse brain before stroke. Infarct size was 1.0 +/- 0.26, 1.19 +/- 0.36, 1.5 +/- 0.36, 1.3 +/- 0.36, and 1.1 +/- 0.28 mm(3), respectively. The increase in infarct size with full-length GADD34 was statistically significant (P < 0.05). Immunohistochemistry confirmed viral protein expression. Tissue culture studies revealed GADD34 gene restored virulence in HSV1716, suggesting that HSV virulence, rather than increased GADD34, exacerbated ischaemic damage.