Spinal cord injury induces upregulation of Beclin 1 and promotes autophagic cell death
Spinal cord injury induces upregulation of Beclin 1 and promotes autophagic cell death
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DOI：
10.1016/j.nbd.2008.09.009
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发表时间：
2009-02-01
影响因子：
6.1
通讯作者：
Itoi, Eiji
中科院分区：
文献类型：
--
作者：
Kanno, Haruo;Ozawa, Hiroshi;Itoi, Eiji
自噬是细胞质的降解，在一些神经退行性疾病中诱导自噬性细胞死亡。Beclin 1是一种与Bcl-2相互作用的蛋白，已知是自噬的启动子。我们使用小鼠脊髓半切模型研究了脊髓损伤后Beclin 1蛋白表达的变化以及自噬和自噬细胞死亡的参与。在本研究中，Beclin 1的表达显着增加，在病变部位后半切。Beclin 1的表达从半切后4 h开始增加，3d达高峰，并持续至少21 d。在神经元、星形胶质细胞和少突胶质细胞中观察到Beclin 1表达。表达Beclin 1的细胞中的细胞核是圆形的，这通常应该在自噬性细胞死亡中观察到，并且它们不像在凋亡细胞核中观察到的那样收缩或碎裂。本研究的结果表明，自噬在损伤的脊髓中被激活。此外，自噬细胞死亡被认为是明确有助于脊髓损伤后的神经组织损伤。(C)2008年爱思唯尔公司All rights reserved.
Autophagy is a degradation of the cytoplasm and it induces autophagic cell death in several neurodegenerative conditions. Beclin 1, a Bcl-2-interacting protein, is known to be a promoter of autophagy. We investigated the alterations in the Beclin 1 protein expression and the involvement of autophagy and autophagic cell death after spinal cord injury using a spinal cord hemisection model in mice. In the present study, the Beclin 1 expression dramatically increased at the lesion site after hemisection. The increased expression of Beclin 1 started from 4 h, peaked at 3 d, and lasted for at least 21 d after hemisection. The Beclin 1 expression was observed in neurons, astrocytes, and oligodendrocytes. The nuclei in the Beclin 1 expressing cells were round, which should normally be observed in autophagic cell death, and they were not either shrunken or fragmented as is observed in apoptotic nuclei. The results of the present study suggested that autophagy is activated in the injured spinal cord. Furthermore, autophagic cell death is considered to clearly contribute to neural tissue damage after spinal cord injury. (C) 2008 Elsevier Inc. All rights reserved.