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MicroRNA expression in rat hippocampus up to 1 year after fluid percussion brain injury

ABSTRACT: microRNA expression in rat hippocampus up to 1 year after fluid percussion brain injury

PROVIDER: PRJNA544477 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9114500.fastq.gz	Fastqsanger.gz
	SRR9114510.fastq.gz	Fastqsanger.gz
	SRR9114520.fastq.gz	Fastqsanger.gz
	SRR9114530.fastq.gz	Fastqsanger.gz
	SRR9114540.fastq.gz	Fastqsanger.gz

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microRNA expression in rat hippocampus up to 1 year after fluid percussion brain injury

Project description:Purpose: The goal of this study is to investigate the expression of microRNAs up to 1 year after fluid percussion TBI Methods: miRNA-Seq analysis of microRNA expression in the hippocampus of TBI and sham surgery rats

2020-03-09 | GSE131704 | GEO

Transcriptional Pathology Evolves Over Time in Rat Hippocampus Following Lateral Fluid Percussion Traumatic Brain Injury

Project description:Traumatic brain injury (TBI) causes acute and lasting impacts on the brain, driving pathology along anatomical, cellular, and behavioral dimensions. Rodent models offer the opportunity to study TBI in a controlled setting, and enable analysis of the temporal progression that occurs from injury to recovery. We applied transcriptomic and epigenomic analysis, characterize gene expression and in ipsilateral hippocampus at 1 and 14 days following moderate lateral fluid percussion (LFP) injury. This approach enabled us to identify differential gene expression (DEG) modules with distinct expression trajectories across the two time points. The major DEG modules represented genes that were up- or downregulated acutely, but largely recovered by 14 days. As expected, DEG modules with acute upregulation were associated with cell death and astrocytosis. Interestingly, acutely downregulated DEGs related to neurotransmission mostly recovered by two weeks. Upregulated DEG modules related to inflammation were not necessarily elevated acutely, but were strongly upregulated after two weeks. We identified a smaller DEG module with delayed downregulation at 14 days including genes related to cholesterol metabolism and amyloid beta clearance. Finally, differential expression was paralleled by changes in H3K4me3 at the promoters of differentially expressed genes at one day following TBI. Following TBI, changes in cell viability, function and ultimately behavior are dynamic processes. Our results show how transcriptomics in the preclinical setting has the potential to identify biomarkers for injury severity and/or recovery, to identify potential therapeutic targets, and, in the future, to evaluate efficacy of an intervention beyond measures of cell death or spatial learning.

2021-10-31 | GSE173975 | GEO

Transcriptional Pathology Evolves Over Time in Rat Hippocampus Following Lateral Fluid Percussion Traumatic Brain Injury

Project description:Transcriptional Pathology Evolves Over Time in Rat Hippocampus Following Lateral Fluid Percussion Traumatic Brain Injury

| PRJNA727795 | ENA

Altered neuroinflammaory transcriptomic profile in the hippocampal dentate gyrus three weeks after lateral fluid percussion injury in rats

Project description:Traumatic brain injury (TBI) is a major source of disability worldwide with cognitive and memory deficits being pervasive after injury. The hippocampus, a major structure involved in learning and memory, is particularly vulnerable to TBI, and cellular dysfunction within the hippocampal dentate gyrus is believed to be a major contributor to cognitive deficits after TBI. However, there is a little known about the transcriptomic changes occurring directly within the dentate gyrus at subacute-to-chronic timepoints after TBI. To address this, we performed bulk RNA sequencing and single nuclei RNA sequencing of the isolated dentate gyrus three weeks after lateral fluid percussion injury in male rats. We report here that there is evidence of an ongoing neuroinflammatory response marked by increased neuroinflammatory genes that implicate various neuroinflammatory pathways that are associated with a subset of microglia and astrocyte populations. R-code available at "https://github.com/NgwenyaLab/DeSana_and_Alfawares_2025"

2025-09-21 | GSE307917 | GEO

Transcription profiling of rat brain time series samples treated with lateral fluid percussion injury or sham surgery without injury to investigate the physiological effects of taumatic brain injury

Project description:Traumatic brain injury (TBI) induces a complex cascade of molecular and physiological effects. This study proposes to investigate the gene expression profile in cortex and hippocampus over early time points, following two different injury severities. These results will complement prior knowledge of both metabolic and neuroplastic changes after TBI, as well as serve as a starting point to investigate additional gene families whose expression is altered after TBI.,To characterize the profile of gene expression following a diffuse traumatic brain injury of varying severity in adult rats. ,Distinct patterns of gene expression following traumatic brain injury will occur in a time- and injury-dependent fashion. In particular, changes in expression of enzymes involved in energy metabolism and neuroplasticity will be detected.,Adult rats will be subjected to mild and severe lateral fluid percussion injury OR sham surgery without injury. At various post-injury timepoints (0.5, 4 and 24 hours), animals will be sacrificed, brain regions (parietal cortex and hippocampus, ipsilateral and contralateral to injury) will be dissected and RNA isolated. RNA will be used to synthesize cRNA probes for microarray hybridization. RNA from 2 matched animals will be pooled onto a single chip (U34A rat, Affymetrix). Comparisons will be made between sham and injured animals, with brain region, injury severity, and post-injury time point as the experimental variables.

2007-07-31 | E-GEOD-2871 | biostudies-arrayexpress

Transcriptomics but not DNA methylomics find Tp73, Cebpd, Pax6 and Spi1 transcription factors as treatment targets for traumatic brain injury

Project description:TBI was induced with lateral fluid-percussion injury in adult male rats. MBD-seq of the perilesional cortex, ipsilateral thalamus and ipsilateral hippocampus was performed at 3 months post-TBI. The data was used to identify differential methylation of gene promoter, gene body, and exons in the perilesional cortex , thalamus and hippocampus.

2018-05-22 | GSE107837 | GEO

Fluid Shear Stress Up-regulates Vascular Endothelial Growth Factor Gene

Project description:Fluid induced shear stress is widely recognized as an important biophysical signal in cell-cell mechanotransduction. To identify cellular signaling pathways that are regulated by fluid shear stress, we applied the unbiased approach of transcriptional profiling. Our cDNA array analysis detected that 1165 of the 6288 sampled unigenes were significantly affected by pulsatile fluid flow. GenMapp 2.1 analysis revealed pathways of genes regulated by shear stress: angiogenesis, blood vessel morphogenesis, regulation of endothelial cell proliferation and prostaglandin biosynthesis. Individual genes significantly up-/down-regulated by shear stress included vascular endothelial growth factor A (VEGFa), cysteine rich protein 61 (CRY61), platelet derived growth factor, alpha (PDGFa), connective tissue growth factor (CTGF), Neuropilin 1 (NRP1), angiotensin II receptor, type 1a (AGTR1a) and fibroblast growth factor 1 (FGF1). Based on these findings, we hypothesize that fluid shear stress regulated VEGF most likely stimulates MC3T3-E1 cells through autocrine/paracrine release and may provide a powerful recruitment signal for osteoclasts, endothelial cells and/or stem cells during bone remodeling. Keywords: stress response

2007-06-20 | GSE8117 | GEO

Gene expression of whole hippocampus 24hr post-injury in rat

Project description:Traumatic brain injury (TBI) alters and dysregulates the expression of thousands of genes in the brain. Since some of the most common problems in TBI patients are learning and memory deficits, we are studying the effects of TBI on the hippocampus, a region of the brain which is essential for learning and memory and which is known to be particularly vulnerable to TBI. We are interested in understanding how potential neuroprotective drugs alter the TBI-induced gene expression profile. The objective of this study is to elucidate and compare the differential gene expression profiles in the hippocampus of naive, sham-control, TBI and TBI plus drug treated rats. JM6, PMI-006 and E33 are three compounds with neuroprotective, anti-inflammatory and anti-oxidative effects. Our goal is to determine if different neuroprotective compounds have similar effects on common gene targets. These genes and the cell signaling pathways linked to them would then be the target of new therapeutic strategies for TBI. Rats were prepared for fluid percussion traumatic brain injury or sham injury (naÃ¯ve rats had no anesthesia and were not handled in any way and gene expression in their brains serve as baseline data) and 24 hr post-injury, hippocampi were obtained, and stored in RNA later. Total RNA was isolated, quantitified and used for Agilent microarray analysis at GenUs Biosystems. Each group of naive, sham control, TBI and TBI plus JM6, TBI plus PMI-006 and TBI plus E33 (estrogen) has three biological replicates.

2015-01-08 | E-GEOD-59645 | biostudies-arrayexpress

Transcriptional Pathology Evolves over Time in Rat Hippocampus after Lateral Fluid Percussion Traumatic Brain Injury.

Project description:Traumatic brain injury (TBI) causes acute and lasting impacts on the brain, driving pathology along anatomical, cellular, and behavioral dimensions. Rodent models offer an opportunity to study the temporal progression of disease from injury to recovery. Transcriptomic and epigenomic analysis were applied to evaluate gene expression in ipsilateral hippocampus at 1 and 14 days after sham (n = 2 and 4, respectively per time point) and moderate lateral fluid percussion injury (n = 4 per time point). This enabled the identification of dynamic changes and differential gene expression (differentially expressed genes; DEGs) modules linked to underlying epigenetic response. We observed acute signatures associated with cell death, astrocytosis, and neurotransmission that largely recovered by 2 weeks. Inflammation and immune signatures segregated into upregulated modules with distinct expression trajectories and functions. Whereas most down-regulated genes recovered by 14 days, two modules with delayed and persistent changes were associated with cholesterol metabolism, amyloid beta clearance, and neurodegeneration. Differential expression was paralleled by changes in histone H3 lysine residue 4 trimethylation at the promoters of DEGs at 1 day post-TBI, with the strongest changes observed for inflammation and immune response genes. These results demonstrate how integrated genomics analysis in the pre-clinical setting has the potential to identify stage-specific biomarkers for injury and/or recovery. Though limited in scope here, our general strategy has the potential to capture pathological signatures over time and evaluate treatment efficacy at the systems level.

| S-EPMC8667199 | biostudies-literature

Altered neuroinflammaory transcriptomic profile in the hippocampal dentate gyrus three weeks after lateral fluid percussion injury in rats

Project description:Altered neuroinflammaory transcriptomic profile in the hippocampal dentate gyrus three weeks after lateral fluid percussion injury in rats

| PRJNA1327799 | ENA

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