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Single moderate traumatic brain injury in mice induces transient acute changes in the cortical iNOS expression and its cytoplasmic co- localization with TDP-43 (CROSBI ID 720171)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | međunarodna recenzija

Janković, Tamara ; Gržeta, Nika ; Dolenec, Petra ; Križ, Jasna ; Pilipović, Kristina Single moderate traumatic brain injury in mice induces transient acute changes in the cortical iNOS expression and its cytoplasmic co- localization with TDP-43 // Inflammation and Proteinopathy in ALS/FTD Spectrum Disorder. 2022. str. 25-26

Podaci o odgovornosti

Janković, Tamara ; Gržeta, Nika ; Dolenec, Petra ; Križ, Jasna ; Pilipović, Kristina

engleski

Single moderate traumatic brain injury in mice induces transient acute changes in the cortical iNOS expression and its cytoplasmic co- localization with TDP-43

Introduction: Traumatic brain injury (TBI) occurs as a consequence of mechanical injury to the brain and is considered to be the leading cause of death and disability in young individuals. Inflammation, one of the secondary injury pathophysiological processes, contributes to posttraumatic brain damage and lifelong cognition and memory impairments. Inducible nitric oxide synthase (iNOS) is a cytoplasmic enzyme that forms the signalling molecule nitric oxide involved in neuroinflammation. In TBI, it has been also shown that mislocalization of TAR DNA-binding protein 43 (TDP-43) contributes to post-injury pathology. We investigated acute changes in the iNOS expression following single moderate TBI in wild-type mice in different brain regions and its colocalization with TDP-43. Materials/Methods: Single moderate lateral fluid percussion injury was induced over the left parietal cortex of the male adult C57BL/J mice. Animals were sacrificed one or three days after TBI and their brains were prepared for Western blot or immunohistological analyses. Animals of the control group were sacrificed 1 day after the sham injury procedure. Results: An increase in the iNOS expression was observed in the ipsilateral cortex one day after the brain trauma. In the tested time points, changes in the iNOS expression were not detected in the ipsilateral hippocampus and contralateral cortex, and hippocampus of traumatized animals. Also, a colocalization of iNOS and TDP-43 in the cytoplasm was observed in the most damaged part of the ipsilateral cortex one day after TBI. Conclusions: Transient acute changes in the proinflammatory marker iNOS in the ipsilateral cortex are induced by single moderate brain trauma. Cytoplasmic colocalization of iNOS and TDP-43 in the most damaged part of the ipsilateral cortex suggests the interconnection of these proteins. This work was supported by the University of Rijeka, Croatia, project number uniri-biomed-18-199 to K.P.

Cortex ; Inducible nitric oxide synthase ; Hippocampus ; Traumatic brain injury

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Podaci o prilogu

25-26.

2022.

objavljeno

Podaci o matičnoj publikaciji

Inflammation and Proteinopathy in ALS/FTD Spectrum Disorder

Podaci o skupu

Inflammation and Proteinopathy in ALS/FTD Spectrum Disorder

poster

30.06.2022-03.07.2022

Rijeka, Hrvatska

Povezanost rada

Biotehnologija u biomedicini (prirodno područje, biomedicina i zdravstvo, biotehničko područje), Temeljne medicinske znanosti