prikaz prve stranice dokumenta Tlr2 deficiency is associated with enhanced elements of neuronal repair and caspase 3 activation following brain ischemia
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Scientific paper - Original scientific paper
Tlr2 deficiency is associated with enhanced elements of neuronal repair and caspase 3 activation following brain ischemia
Scientific Reports, 9 (2019), 1; 2821. https://doi.org/10.1038/s41598-019-39541-3
Gorup, Dunja; Škokić, Siniša; Križ, Jasna; Gajović, Srećko

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Gorup, D., Škokić, S., Križ, J. & Gajović, S. (2019). Tlr2 deficiency is associated with enhanced elements of neuronal repair and caspase 3 activation following brain ischemia. Scientific Reports, 9. (1), 2821. doi: 10.1038/s41598-019-39541-3

Gorup, Dunja, et al. "Tlr2 deficiency is associated with enhanced elements of neuronal repair and caspase 3 activation following brain ischemia." Scientific Reports, vol. 9, no. 1, 2019, p. 2821. https://doi.org/10.1038/s41598-019-39541-3

Gorup, Dunja, Siniša Škokić, Jasna Križ and Srećko Gajović. "Tlr2 deficiency is associated with enhanced elements of neuronal repair and caspase 3 activation following brain ischemia." Scientific Reports 9, no. 1 (2019): 2821. https://doi.org/10.1038/s41598-019-39541-3

Gorup, D., et al. (2019) 'Tlr2 deficiency is associated with enhanced elements of neuronal repair and caspase 3 activation following brain ischemia', Scientific Reports, 9(1), p. 2821. doi: 10.1038/s41598-019-39541-3

Gorup D, Škokić S, Križ J, Gajović S. Tlr2 deficiency is associated with enhanced elements of neuronal repair and caspase 3 activation following brain ischemia. Scientific Reports [Internet]. 2019 February 26 [cited 2024 November 22];9(1):2821. doi: 10.1038/s41598-019-39541-3

D. Gorup, S. Škokić, J. Križ and S. Gajović, "Tlr2 deficiency is associated with enhanced elements of neuronal repair and caspase 3 activation following brain ischemia", Scientific Reports, vol. 9, no. 1, p. 2821, February 2019. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:105:900098. [Accessed: 22 November 2024]

Metadata
Title (english)Tlr2 deficiency is associated with enhanced elements of neuronal repair and caspase 3 activation following brain ischemia
AuthorDunja Gorup
AuthorSiniša Škokić
AuthorJasna Križ
AuthorSrećko Gajović
Author's institutionUniversity of Zagreb
School of Medicine
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
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 type controls. Altered inflammation in Tlr2-deficient mice was accompanied by enhanced elements of post-stroke repair, in particular during the chronic phase of recovery, but also with delayed final consolidation of the brain lesion.
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review
Publication versionPublished version
Journal titleScientific Reports
Numberingvol. 9, no. 1, p. 2821
p-ISSN2045-2322
DOIhttps://doi.org/10.1038/s41598-019-39541-3
URN:NBNurn:nbn:hr:105:900098
Publication2019-02-26
Document URLhttp://doi.org/10.1038/s41598-019-39541-3
Type of resourceText
Access conditionsOpen access
Terms of useLicence In copyright icon
Created on2024-03-28 10:27:04