Changes in autophagy proteins in a rat model of controlled cortical impact induced brain injury

被引:62
作者
Sadasivan, Shankar [2 ]
Dunn, William A., Jr. [3 ,4 ]
Hayes, Ronald L. [1 ,5 ]
Wang, Kevin K. W. [1 ]
机构
[1] Banyan Biomarkers Inc, Ctr Innovat Res, Alachua, FL 32615 USA
[2] Univ Florida, Dept Psychiat, Gainesville, FL 32610 USA
[3] Univ Florida, Dept Anat, Gainesville, FL 32610 USA
[4] Univ Florida, Dept Cell Biol, Gainesville, FL 32610 USA
[5] Univ Florida, Dept Anesthesiol, Gainesville, FL 32610 USA
关键词
traumatic brain injury; autophagy; beclin-1-bcl-2; ratio; MAP-LC3;
D O I
10.1016/j.bbrc.2008.05.031
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Autophagy has been implicated in several neurodegenerative diseases and recently its role in acute brain injury has received increased interest. In our study, we investigated the profiles of autophagy-linked proteins (MAP-LC3 (Atg8), beclin-1 (Atg6) and the beclin-1-binding protein, bcl-2, following controlled cortical impact injury in rats-a model for moderate-to-severe traumatic brain injury. We observed significant increases in the levels of the processed form of LC3 (LC3-II) in the ipsilateral cortex 2 h to 2 days after injury when compared to sham. Furthermore, the beclin-1/bcl-2 ratio in the ipsilateral cortex was found to have increased from 1 and 2 days after injury. Since both of these changes are established autophagy-enabling events, and, based on these data, we propose that autophagy, plays a role in the manifestation of cell injury following brain trauma. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:478 / 481
页数:4
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