Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse

•GAP43 and CASP3 are primarily present in neurons after stroke.•Expression of Gap43 and Casp3 increased after onset of stroke.•GAP43 and CASP3 colocalized after onset of stroke. GAP43 is a protein involved in neurite outgrowth during development and axon regeneration reflecting its presynaptic local...

Full description

Saved in:
Bibliographic Details
Published in:Neuroscience letters 2015-06, Vol.597, p.176-182
Main Authors: Gorup, Dunja, Bohaček, Ivan, Miličević, Tena, Pochet, Roland, Mitrečić, Dinko, Križ, Jasna, Gajović, Srećko
Format: Article
Language:English
Subjects:
Animals
Astrocytes - metabolism
Bioluminescence
Brain - metabolism
Brain ischemia
Brain Ischemia - metabolism
CASP3
Caspase 3 - metabolism
GAP-43 Protein - metabolism
GAP43
Mice, Inbred C57BL
Mice, Transgenic
Neurons - metabolism
Time Factors
tMCAO
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:•GAP43 and CASP3 are primarily present in neurons after stroke.•Expression of Gap43 and Casp3 increased after onset of stroke.•GAP43 and CASP3 colocalized after onset of stroke. GAP43 is a protein involved in neurite outgrowth during development and axon regeneration reflecting its presynaptic localization in developing neurons. Recently, it has been demonstrated that GAP43 is a ligand of CASP3 involved in receptor endocytosis and is also localized post-synaptically. In this study, by using a transgenic mouse strain carrying a bioluminescent reporter for GAP43 combined with an in vivo bioluminescence assay for CASP3, we demonstrated that one day after brain ischemic lesion and, even more pronounced, four days after stroke, expression of both CASP3 and Gap43 in neurons increased more than 40 times. The in vivo approach of CASP3 and GAP43 colocalization imaging was further validated and quantified by immunofluorescence. Importantly, in 82% of GAP43 positive cells, colocalization with CASP3 was present. These findings suggested that one and four days after stroke CASP3 expression, not necessarily associated with neuronal death, increased and suggested that CASP3 and GAP43 might be part of a common molecular pathway involved in early response to ischemic events occurring after onset of stroke.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2015.04.042