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

Tony Frugier; Juliet M Taylor; Catriona McLean; Nicole Bye; Philip M Beart; Rodney J Devenish; Peter J Crack

doi:10.1016/j.neuint.2016.02.016

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

Neurochem Int. 2016 Jun:96:62-8. doi: 10.1016/j.neuint.2016.02.016. Epub 2016 Feb 27.

Authors

Tony Frugier¹, Juliet M Taylor¹, Catriona McLean², Nicole Bye³, Philip M Beart⁴, Rodney J Devenish⁵, Peter J Crack⁶

Affiliations

¹ Department of Pharmacology & Therapeutics, University of Melbourne, Parkville, Australia.
² Department of Anatomical Pathology, The Alfred Hospital, Melbourne, Australia.
³ Department of Anatomy and Neuroscience, University of Melbourne, Parkville, Australia.
⁴ Department of Pharmacology & Therapeutics, University of Melbourne, Parkville, Australia; Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Australia.
⁵ Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Clayton Campus, Victoria, Australia.
⁶ Department of Pharmacology & Therapeutics, University of Melbourne, Parkville, Australia. Electronic address: pcrack@unimelb.edu.au.

PMID: 26930584
DOI: 10.1016/j.neuint.2016.02.016

Abstract

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 post-mortem tissue observed an increase in staining in microtubule-associated protein 1 light chain 3 (LC3), sequestosome 1 (SQSTM1; 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.

Keywords: Autophagy; Brain; Human; LC3; P62; Stroke.

MeSH terms

Aged
Aged, 80 and over
Autophagy / physiology*
Beclin-1 / analysis
Beclin-1 / biosynthesis*
Brain / metabolism*
Brain / pathology
Brain Chemistry / physiology
Female
Humans
Male
Microtubule-Associated Proteins / analysis
Microtubule-Associated Proteins / biosynthesis*
Sequestosome-1 Protein / analysis
Sequestosome-1 Protein / biosynthesis*
Stroke / metabolism*
Stroke / pathology

Substances

BECN1 protein, human
Beclin-1
MAP1LC3A protein, human
Microtubule-Associated Proteins
SQSTM1 protein, human
Sequestosome-1 Protein