Evidence for the recruitment of autophagic vesicles in human brain after stroke

被引:17
|
作者
Frugier, Tony [1 ]
Taylor, Juliet M. [1 ]
McLean, Catriona [2 ]
Bye, Nicole [3 ]
Beart, Philip M. [1 ,4 ]
Devenish, Rodney J. [5 ,6 ]
Crack, Peter J. [1 ]
机构
[1] Univ Melbourne, Dept Pharmacol & Therapeut, Parkville, Vic 3052, Australia
[2] Alfred Hosp, Dept Anat Pathol, Melbourne, Vic, Australia
[3] Univ Melbourne, Dept Anat & Neurosci, Parkville, Vic 3052, Australia
[4] Univ Melbourne, Florey Inst Neurosci & Mental Hlth, Parkville, Vic 3052, Australia
[5] Monash Univ, Biomed Discovery Inst, Clayton Campus, Melbourne, Vic, Australia
[6] Monash Univ, Dept Biochem & Mol Biol, Clayton Campus, Melbourne, Vic, Australia
基金
英国医学研究理事会; 澳大利亚研究理事会;
关键词
Autophagy; Stroke; Human; Brain; LC3; P62; CEREBRAL-ISCHEMIA; NEURON DEATH; RAT MODEL; INJURY; INVOLVEMENT; CONTRIBUTES; ACTIVATION; P62;
D O I
10.1016/j.neuint.2016.02.016
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 is a homeostatic process for recycling proteins and organelles that is increasingly being proposed as a therapeutic target for acute and chronic neurodegenerative diseases, including stroke. Confirmation that autophagy is present in the human brain after stroke is imperative before prospective therapies can begin the translational process into clinical trials. Our current study using human postmortem tissue observed an increase in staining in microtubule-associated protein 1 light chain 3 (LC3), sequestosome 1 (SQSTMI; also known as p62) and the increased appearance of autophagic vesicles after stroke. These data confirm that alterations in autophagy take place in the human brain after stroke and suggest that targeting autophagic processes after stroke may have clinical significance. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:62 / 68
页数:7
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