Similar Datasets
Project description:Timecourse RNAseq for Drosophila TBI
| PRJNA718601 | ENA
Project description:Traumatic brain injury (TBI) causes hospitalizations and mortality worldwide with no approved neuroprotective treatments available, partly due to a poor understanding of the molecular mechanisms underlying TBI neuropathology and neuroprotection. We previously reported that the administration of low-dose methamphetamine (MA) induced significant functional/cognitive improvements following severe TBI in rats. We further demonstrated that MA mediates neuroprotection in part, via dopamine-dependent activation of the PI3K-AKT pathway. Here, we further investigated the proteomic changes within the rat cortex and hippocampus following mild TBI (TM), severe TBI (TS), or severe TBI plus MA treatment (TSm) compared to sham operated controls (n=78 in total). We quantified >7,000 unique proteins in total and identified 402 and 801 altered proteins (APs) with high confidence in cortical and hippocampal tissues, respectively. The overall profile of APs observed in TSm rats more closely resembled those seen in TM rather than TS rats. Pathway analysis suggested beneficial roles for acute signaling through IL-6, TGFβ, and IL-1β. Moreover, changes in fibrinogen levels observed in TSm rats suggested a potential role for these proteins in reducing/preventing TBI-induced coagulopathies. These data facilitate further investigations to identify specific pathways and proteins that may serve as key targets for the development of neuroprotective therapies.
2021-03-02 | PXD024317 | Pride
Project description:Using 10x Genomics' single-cell RNA-seq (scRNA-seq) technology, we profiled expression of genes in cell type-specific MAGL knockout mice that received TBI. We found that there are differences in expression of genes between WT, tKO, nKO, and aKO mice in sham or TBI.
2021-06-22 | GSE178226 | GEO
Project description:The variations of psycho- and physiological deficits caused by TBI correlate with the degree of brain injury. However, the objective stratification of TBI is yet elusive. A modified closed-head injury Marmarou model was used based on the release of a 500 gram steel slug on top of the rat skull from a height of 100 cm or 120 cm to induce differential injury models for mild TBI and moderate TBI, respectively. The skull was covered by a helmet to mimic the warfighter’s condition in theater. The hippocampus was at the focal point of injury, and the cerebellum, was susceptible to diffused shock (secondary injury). The HC-CB axis coordinates visuomotor performance, which is known to be vulnerable to TBI. The rats that received moderate TBI showed deficient visuomotor performance by the Barnes maze test for longer time periods than those inflicted with mild TBI. The time resolved and HC-CB specific transcriptomic analysis focused on genes that enabled discrimination of mild from moderate TBI at 14d post injury which is equivalent to nearly 1.5 years of human lifetime. The functional analysis elucidated an active healing mechanism in the HC exposed to mild TBI. In contrast, moderate TBI caused delayed healing and active cell death in the HC. In conclusion, the graded brain injuries differentially implicated the HC-CB axis, despite the use of a helmet to reduce the impact. Time resolved functional dynamics informed the distinct consequences of mild vs. moderate TBI.
2020-12-31 | GSE131435 | GEO
Project description:Glial immune-related pathways as mediators of closed head TBI effects on behavior and lethality in Drosophila
| PRJNA690250 | ENA
Project description:Purpose: Post-traumatic epilepsy (PTE) is an epilepsy that develops after traumatic brain injury (TBI), and it comprises 10-20% of structural epilepsies and 5% of all epilepsies. The lack of prognostic biomarkers for PTE hinders the development of anti-epileptogenic treatments. In this preclinical multicenter study, plasma samples collected from a rat model of PTE were analyzed by small RNA sequencing to reveal the post-TBI expression profile of circulating microRNAs and to identify potential miRNA biomarkers for PTE development. Methods: The animal experiments were conducted at 3 different study sites: University of Eastern Finland (Finland), Monash University (Australia), and University of California, Los Angeles (USA). Severe TBI was induced in adult male Sprague-Dawley rats by the lateral fluid-percussion injury (LFPI) method. Rats that developed PTE were identified by video-EEG monitoring during the 7th post-injury month (TBI rats with epilepsy, TBIE; TBI rats without epilepsy, TBIN). Small RNA sequencing was conducted with plasma samples collected 48 hours after TBI or sham operation (craniotomy). Following the primary quantification, DESeq2 (v. 1.42.0) was used to identify differentially expressed miRNAs between the experiment groups. Results were further validated in a larger sample cohort by droplet digital PCR (ddPCR). Results: Small RNA sequencing detected a total of 754 miRNAs that were expressed in at least one sample. DESeq2 detected 23 differentially expressed (DE) miRNAs between the TBI and sham groups, 12 between the TBIE and sham groups, and 5 between the TBIN and sham groups. In contrast, no DE miRNAs were detected between the TBIE and TBIN groups. From the list of 23 DE miRNAs between the TBI and sham groups, 3 upregulated miRNAs (rno-miR-183-5p, rno-miR-323-3p, and miR-434-3p) were selected for further ddPCR validation. The list of miRNAs for validation was further complemented by 4 miRNAs (rno-miR-9a-3p, rno-miR-124-3p, rno-miR-132-3p, and rno-miR-212-3p), which were not differentially expressed in the DESeq2 analysis, but which we have previously detected to be acutely upregulated in TBI rat plasma. The validation was conducted with samples from the entire EpiBioS4Rx cohort [26 baseline samples, 45 sham, 164 TBI (32 TBIE, 132 TBIN)]. DdPCR analysis revealed that all 7 investigated miRNAs were upregulated in the TBI rats compared with the sham controls. No differences were detected between the rats with (TBIE) or without epilepsy (TBIN). In contrast, TBIE rats that had seizure clusters (severe PTE) had lower levels of plasma miR-212-3p compared with other TBI rats. Furthermore, elastic net regularized logistic regression (glmnet) analysis identified miR-212-3p and miR-132-3p as the optimal set to differentiate TBIE rats with seizure clusters from other TBI rats. Conclusions: The profile of circulating plasma microRNAs differed between TBI rats and sham controls. MiR-212-3p alone or in combination with miR-132-3p showed potential as prognostic biomarkers for development of severe PTE.
2024-12-12 | GSE279767 | GEO
Project description:Tissue damage precedes GvHD and the events leading up to this inflammatory disease are not well understood. To identify cell populations that may invade the intestinal tract after total body irradiation (TBI), we performed a microarray based gene expression analysis of the intestinal tract isolated from untreated mice or mice that had received 9 Gray TBI 24 h or 48 h previously. The aim of the microarray based gene expression analysis was to identify genes specific for certain cell populations that may contribute to GvHD.
2014-04-28 | E-MTAB-1566 | biostudies-arrayexpress
Project description:RNAseq was performed from Drosophila head tissue of two mitochondrial complex I deficiency models. The NDUFS1 homolog ND-75 was knocked down in Drosophila neurons using nSybGal4. Heads were collected from control of ND-75 knockdown flies and used for RNAseq analysis.
2023-12-01 | GSE248363 | GEO
Project description:RNAseq was performed from Drosophila head tissue of a mitochondrial complex I deficiency model. The NDUFS1 homolog ND-75 was knocked down in Drosophila neurons using nSybGal4. Heads were collected from control of ND-75 knockdown flies and used for RNAseq analysis.
2022-10-07 | GSE214562 | GEO
Project description:Traumatic brain injury (TBI) can cause persistent pathological alteration of neurons. This may lead to cognitive dysfunctions, depression, and even increased susceptibility to life threatening diseases, such as epilepsy. To investigate the underlying genetic and molecular basis of TBI, Wasserman and colleagues developed an inexpensive and reproducible model for simulating TBI in Drosophila melanogaster (Fruit Fly). Using a modified version of this model, we subjected w1118 fruit flies to mild closed head trauma. To determine the transcriptomic changes which contribute to survival post TBI, we collected fly heads from the survivors at 2 time points; 4 hours and 24 hours post-trauma. We observed that the induction of transcriptomic changes occur 24 hours post-trauma in fly heads. Classification of these AS changes showed selective retention of long introns (>81bps), with a mean size of ~3000bps. Gene ontology analysis of the genes containing retained introns showed significant enrichment for critical regulators of glycolysis, citric acid cycle as well as vesicle mediated neurotransmitter release. Some of these genes also showed a significant reduction in transcript abundance. The retained introns were enriched for CA-rich motifs known to bind to Smooth (SM), an hnRNPL class of splicing factor.
2017-09-22 | GSE104100 | GEO