The dentate gyrus after traumatic brain injury [mRNA]
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE86579 | GEO | 2017/02/25
SECONDARY ACCESSION(S): PRJNA342298
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of the dentate gyrus of traumatic brain injury model. Results provide insight into the molecular mechanism underlying TBI.
2017-02-25 | GSE86614 | GEO
Project description:The dentate gyrus after traumatic brain injury
| PRJNA342409 | ENA
Project description:Background: Traumatic brain injury (TBI) often results in diverse molecular responses, challenging traditional proteomic studies that measure average changes at tissue levels and fail to capture the complexity and heterogeneity of the affected tissues. Spatial proteomics offers a solution by providing insights into sub-region-specific alterations within tissues. This study focuses on the hippocampal sub-regions, analyzing proteomic expression profiles in mice at the acute (1 day) and subacute (7 days) phases of post-TBI to understand subregion-specific vulnerabilities and long-term consequences. Methods: Three mice brains were collected from each group including Sham, 1-day post-TBI and 7-day post-TBI. Hippocampal subregions were extracted using Laser Microdissection (LMD); and subsequently analyzed by label-free quantitative proteomics. Results: The spatial analysis reveals region-specific protein abundance changes, highlighting the elevation of FN1, LGALS3BP, HP, and MUG-1 in the stratum moleculare (SM), suggesting potential immune cell enrichment post-TBI. Notably, established markers of chronic traumatic encephalopathy, IGHM and B2M, exhibit specific upregulation in the dentate gyrus bottom (DG2) independent of direct mechanical injury. Metabolic pathway analysis identifies disturbances in glucose and lipid metabolism, coupled with activated cholesterol synthesis pathways enriched in SM at 7-Day post-TBI and subsequently in deeper DG1 and DG2 suggesting a role in neurogenesis and onset of recovery. Coordinated activation of neuroglia and microtubule dynamics in DG2 suggest recovery mechanisms in less affected regions. Cluster analysis revealed spatial variations post-TBI, indicative of dysregulated neuronal plasticity and neurogenesis and further predisposition to neurological disorders. TBI-induced protein upregulation (MUG-1, PZP, GFAP, TJP, STAT-1 and CD44) across hippocampal sub-regions indicates shared molecular responses and links to neurological disorders. Spatial variations were demonstrated by proteins dysregulated in both or either of the time-points exclusively in each subregion (ELAVL2, CLIC1 in PL, CD44 and MUG-1 in SM, and SHOC2, LGALS3 in DG). Conclusions: Utilizing advanced spatial proteomics techniques, the study unveils the dynamic molecular responses in distinct hippocampal subregions post-TBI. It uncovers region-specific vulnerabilities and dysregulated neuronal processes, and potential recovery-related pathways that contribute to our understanding of TBI’s neurological consequences and provides valuable insights for biomarker discovery and therapeutic targets.
2024-06-23 | PXD051093 | Pride
Project description:Genetic factors are believed to be of importance for outcome of traumatic brain injury (TBI). However, so far mainly allelic variation in apolipoprotein E4 has been studied in human TBI. In order to study the role of genetic factors in experimental TBI, we examined parental DA and PVG strains before and after TBI. A standardized weight drop injury was used and the pericontusional area was dissected 1 day after TBI and transcriptional profiling was performed.
2012-09-06 | E-MTAB-795 | biostudies-arrayexpress
Project description:This project continues our acute TBI studies and initiates chronic studies -- characterizing the temporal genomic profile of the injured brain up to 12 months post-TBI. Thus, the primary objective of this proposal is to determine the long-term effects of traumatic brain injury on gene expression in the hippocampus and cortex, two brain regions known to be particularly vulnerable to TBI.
2018-09-01 | GSE111452 | GEO
Project description:Time dependent-profiles in the gene expression level following lateral moderate fluid percussion injury in the rat brain We used microarray to elucidate relationship between the alteration of gene expression levels and the progression of brain damages following traumatic brain injury. To examine the levels of gene expression in the early phase of traumatic brain injury, we analyzed the gene expression at 3, 6, 12, and 48 h after trauma using the lateral moderate fluid percussion TBI model. The ratios of the gene expression level were compared between chips corresponding to the 3, 6 and 12 h fluid percussion groups and the sham group chips. On the other hand, the rations of gene expression level after 48 h FPI were compared with 48 h sham chip, because the gene expression levels of 48 h sham chip were distinct from sham group chips (3, 6 and 12 h) in the cluster and principal components analyses.
2010-12-07 | E-GEOD-24047 | biostudies-arrayexpress
Project description:Traumatic brain injury (TBI) is an under-recognizedpublic healththreat. Even mild brain injuries can lead to long-term neurologic impairment.Microgliaplay a fundamental role in the development and progression of this ensuing neurologic impairment. Despite this, a microglia-specific injury signature has yet to be identified. We hypothesized that TBI would lead to long-term changes in the transcriptional profile of microglial pathways associated with the development of subsequent neurologic impairment.
2023-12-11 | GSE249918 | GEO
Project description:It is clinically known, that patients often develop osteoporosis following traumatic brain injury (TBI). To enable a better understanding of the underlying mechanism, we developed a murine TBI model. Mice received a controlled cortical impact inducing a TBI. Expression analysis of the femur 3 days following the injury should reveal the regulated genes. We observed a strong downregulation of osteoblast genes, suggesting an inhibition of bone formation. Furthermore, the beta2-adrenoreceptor was downregulated, what is supposed to be induced by the increased adrenergic signaling in these mice.
2024-01-17 | GSE253133 | GEO
Project description:Post-traumatic neuroinflammation is a key driver of secondary injury after traumatic brain injury (TBI). Pyroptosis, a proinflammatory form of programmed cell death, considerably activates strong neuroinflammation and amplifies the inflammatory response by releasing inflammatory contents. Therefore, treatments targeting pyroptosis may beneficially effects for the treatment of secondary brain damage after TBI. Herein, a cysteine-alanine-glutamine-lysine (CAQK) peptide-modified β-lactoglobulin (β-LG) nanoparticle was constructed to deliver disulfiram (DSF), C-β-LG/DSF, to inhibit pyroptosis and decrease neuroinflammation, thereby preventing TBI-induced secondary injury. In the post-TBI mice model, C-β-LG/DSF selectively targets the injured brain, increases DSF accumulation, and extends the time of the systemic circulation of DSF. C-β-LG/DSF can alleviate brain edema and inflammatory response, inhibit secondary brain injury, promote learning, and improve memory recovery in mice after trauma. Therefore, this study likely provided a new approach for reducing the secondary spread of TBI.
2024-01-17 | GSE244966 | GEO
Project description:The developing mouse dentate gyrus
| PRJNA453793 | ENA