Akt phosphorylation and neuronal survival after traumatic brain injury in mice
Akt phosphorylation and neuronal survival after traumatic brain injury in mice
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DOI：
10.1006/nbdi.2002.0482
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发表时间：
2002-04-01
影响因子：
6.1
通讯作者：
Chan, PH
中科院分区：
文献类型：
--
作者：
Noshita, N;Lewén, A;Chan, PH
丝氨酸-苏氨酸激酶Akt参与许多细胞系统的生存信号通路。本研究检测了小鼠创伤性脑损伤（TBI）后Akt丝氨酸-473位点磷酸化和DNA断裂。免疫组化结果显示，在脑损伤后1小时，磷酸化akt在损伤皮质中表达减少，而在4小时时，磷酸化akt在焦周损伤皮质中表达暂时升高。脑损伤后海马CA1区磷酸化akt水平升高。Western blot分析显示，早在创伤后1 h， Akt就显著降低；然而，磷酸化在4 h时加速。phospho-Akt和phospho-BAD或phospho-GSK-3beta双染色显示磷酸化akt和下游元件共定位。磷酸化akt和末端脱氧核苷酸转移酶介导的尿苷5'-三磷酸-生物素缺口末端标记双染色显示TBI后细胞分布不同。本研究提示Akt磷酸化参与脑外伤后细胞存活的信号通路。(C) 2002 Elsevier Science （USA）。
The serine-threonine kinase, Akt, is involved in the survival signaling pathways in many cell systems. The present study examined phosphorylation of Akt at serine-473 and DNA fragmentation after traumatic brain injury (TBI) in mice. Immunohistochemistry showed phospho-Akt was decreased in the injured cortex 1 h after TBI, whereas it was temporally increased at 4 h in the perifocal damaged cortex. In the CA1 region of the hippocampus, phospho-Akt was increased after TBI. Western blot analysis showed that Akt was significantly decreased as early as 1 h after trauma; however, the phosphorylation was accelerated at 4 h. Double staining with phospho-Akt and phospho-BAD or phospho-GSK-3beta revealed the colocalization of phospho-Akt and downstream elements. Double staining with phospho-Akt and terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labeling showed different cellular distributions after TBI. The present study implicates Akt phosphorylation in the signaling pathways that are involved in cell survival after TBI. (C) 2002 Elsevier Science (USA).