Sortilin is dispensable for secondary injury processes following traumatic brain injury in mice
| dc.contributor.author | Staib-Lasarzik, Irina | |
| dc.contributor.author | Gölz, Christina | |
| dc.contributor.author | Bobkiewiecz, Wieslawa | |
| dc.contributor.author | Somnuke, Pawit | |
| dc.contributor.author | Sebastiani, Anne | |
| dc.contributor.author | Thal, Serge C. | |
| dc.contributor.author | Schäfer, Michael K. E. | |
| dc.date.accessioned | 2024-12-20T06:40:31Z | |
| dc.date.available | 2024-12-20T06:40:31Z | |
| dc.date.issued | 2024 | |
| dc.description.abstract | Traumatic brain injury (TBI) is characterized by complex secondary injury processes involving the p75 neurotrophin receptor (p75NTR), which has been proposed as a possible therapeutic target. However, the pathogenic role of the p75NTR co-receptor sortilin in TBI has not been investigated. In this study, we examined whether sortilin contributes to acute and early processes of secondary injury using a murine controlled cortical impact (CCI) model of TBI. Initial expression analysis showed a down-regulation of sortilin mRNA levels 1 and 5 day post injury (dpi) and a reduced expression of sortilin protein 1 dpi. Next, a total of 40 SortilinΔExon14 loss-of-function mouse mutants (Sort1−/−) and wild-type (Sort1+/+) littermate mice were subjected to CCI and examined at 1 and 5 dpi. Neither sensorimotor deficits or brain lesion size nor CCI-induced cell death or calcium-dependent excitotoxicity as evaluated by TUNEL staining or Western blot analysis of alpha II spectrin breakdown products were different between Sort1 | en_GB |
| dc.identifier.doi | http://doi.org/10.25358/openscience-11167 | |
| dc.identifier.uri | https://openscience.ub.uni-mainz.de/handle/20.500.12030/11188 | |
| dc.language.iso | eng | de |
| dc.rights | CC-BY-4.0 | * |
| dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | * |
| dc.subject.ddc | 610 Medizin | de_DE |
| dc.subject.ddc | 610 Medical sciences | en_GB |
| dc.title | Sortilin is dispensable for secondary injury processes following traumatic brain injury in mice | en_GB |
| dc.type | Zeitschriftenaufsatz | de |
| jgu.journal.issue | 15 | de |
| jgu.journal.title | Heliyon | de |
| jgu.journal.volume | 10 | de |
| jgu.organisation.department | FB 04 Medizin | de |
| jgu.organisation.name | Johannes Gutenberg-Universität Mainz | |
| jgu.organisation.number | 2700 | |
| jgu.organisation.place | Mainz | |
| jgu.organisation.ror | https://ror.org/023b0x485 | |
| jgu.pages.alternative | e35198 | de |
| jgu.publisher.doi | 10.1016/j.heliyon.2024.e35198 | de |
| jgu.publisher.issn | 2405-8440 | de |
| jgu.publisher.name | Elsevier | de |
| jgu.publisher.place | London | de |
| jgu.publisher.year | 2024 | |
| jgu.rights.accessrights | openAccess | |
| jgu.subject.ddccode | 610 | de |
| jgu.subject.dfg | Lebenswissenschaften | de |
| jgu.type.contenttype | Scientific article | de |
| jgu.type.dinitype | Article | en_GB |
| jgu.type.resource | Text | de |
| jgu.type.version | Published version | de |