Tlr2 Deficiency is Associated with Enhanced Elements of Neuronal Repair and Caspase 3 Activation Following Brain Ischemia

Scientific Reports
D GorupSrećko Gajović

Abstract

The aim of this study was to apply multimodal in vivo imaging to assess the influence of altered innate immunity on brain repair after ischemic lesion. Tlr2-deficient mice were compared to wild type controls, as they lack Tlr2-mediated pro-inflammatory signaling triggered by postischemic necrosis. The ischemic lesion was induced by transient middle cerebral artery occlusion for 60 min, followed by brain imaging and analysis at four time points until 28 days after ischemia. Multimodal in vivo imaging involved a combination of 3 modalities: (1) magnetic resonance imaging by T2-weighted scans to assess brain lesion size, (2) bioluminescence imaging of Gap43-luc/gfp transgenic mice to visualize the axonal remodeling, and (3) caged-luciferin bioluminescence imaging of DEVD-luciferin allowing for visualization of caspase 3 and 7 activity in Gap43-luc/gfp mice. This enabled innovative correlation of the MRI-determined lesion size to photon fluxes obtained by bioluminescence imaging. Our data revealed that following ischemia, Tlr2-deficient mice had higher Gap43 expression and higher levels of caspases 3 and 7 activity, which was accompanied by enhanced levels of synaptic plasticity markers DLG4 and synaptophysin when compared to wild ...Continue Reading

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Citations

Aug 25, 2021·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Laura SkukanSrećko Gajović

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Methods Mentioned

BETA
transgenic
transgenics

Software Mentioned

TurboRARE
Living Image
MAPSHIM
Image Lab
ImageJ1
Paravision
VivoGlo

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