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Real-time quantitative PCR analysis of rat's brain mRNAs

ABSTRACT: We investigated the therapeutic effect of the extracellular vesicles secreted by glial progenitor cells (GPC-EV) derived from human induced pluripotent stem cell in a traumatic brain injury model. The injury was modeled using the dosed concussion to the open brain method. The male Wistar rats were performed traumatic brain injury (TBI), and after 24 hours animals were randomly divided into two groups: group 1 — rats with intranasal administration of PBS (control), and group 2 — rats with similar administration of extracellular visicles (EV) derived from glial progenitor cells. PCR analysis of brain tissues ( cortex, striatum, hippocampus) were performed on postoperative day 7 and 14 to investigate genes associated with apoptosis, and inflammation.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE242996 | GEO | 2023/09/13

REPOSITORIES: GEO

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Real-time quantitative PCR analysis of rat's brain miRNAs

Project description:We investigated the therapeutic effect of the extracellular vesicles secreted by glial progenitor cells (GPC-EV) derived from human induced pluripotent stem cell in a traumatic brain injury model. The injury was modeled using the dosed concussion to the open brain method. The male Wistar rats were performed traumatic brain injury (TBI), and after 24 hours animals were randomly divided into two groups: group 1 — rats with intranasal administration of PBS (control), and group 2 — rats with similar administration of extracellular visicles (EV) derived from glial progenitor cells. miRNA PCR analysis of brain tissues ( cortex, striatum, hippocampus) were performed on postoperative day 7 to investigate miRNA associated with apoptosis, and inflammation.

2023-09-15 | GSE242828 | GEO

Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (TBI – MBD-seq)

Project description:Explore DNA methylation in traumatic brain injury model of epilepsy and its relationship to gene expression. Examination of methylation changes in stimulated rats compared to sham operated animals in traumatic brain injury model of epilepsy.

2016-09-06 | E-GEOD-75119 | biostudies-arrayexpress

Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (TBI â mRNA-seq)

Project description:Explore DNA methylation in traumatic brain injury model of epilepsy and its relationship to gene expression. Examination of expression changes in stimulated rats compared to sham operated animals in traumatic brain injury model of epilepsy.

2016-09-06 | E-GEOD-75120 | biostudies-arrayexpress

Gene expression file at single cell level of nerve cells in damaged areas of the cerebral cortex in mice with traumatic brain injury

Project description:Endothelial cells-derived extracellular vesicles can promote nerve function in mice with traumatic brain injury. We used snRNAseq to analyze the effects of extracellular vesicles derived from endothelial cells on nerve cells in mice with traumatic brain injury.

2024-09-04 | GSE276065 | 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

Comprehensive analysis of circRNA expression profiles in rat cerebral cortex after moderate traumatic brain injury

Project description:Background: Traumatic brain injury is a medical event of global concern, and a growing body of research suggests that circular RNA can play very important roles in traumatic brain injury. To explore the functions of more novel and valuable circular RNA in traumatic brain injury response, a moderate traumatic brain injury in rat was established and a comprehensive analysis of circular RNA expression profiles in rat cerebral cortex was done. Results: As a result, 301 up-regulated and 284 down-regulated circular RNAs were obtained in moderate traumatic brain injury rats, the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were performed based on the circular RNA’s host genes, and a circRNA-miRNA interaction network based on differentially expressed circular RNAs was constructed. Also, four circular RNAs were validated by RT-qPCR and sanger sequencing. Conclusion: This study showed that differentially expressed circular RNAs existed between rat cerebral cortex after moderate traumatic brain injury and control. And this will provide valuable information for circular RNA research in the field of traumatic brain injury.

2022-01-15 | GSE193521 | GEO

Senolytics improve the neurogenic potential of non-glial progenitors and neurorepair in the dorsal pallium of aged killifish independent of inflammation

Project description:With advancing age, senescent cells accumulate as they are not efficiently cleared by the immune system anymore. Via a senescence-associated secretory phenotype, chronic senescent cells alter the microenvironment, creating an unfavorable milieu for neurogenesis and neurorepair. Using an innovative and rapid aging model, the African turquoise killifish, we have previously demonstrated a dramatic decline in neurogenic potential of non-glial progenitors with age. Even after traumatic brain injury, progenitor proliferation and neuron production was very low in aged killifish in comparison to young adult killifish, and overall neurorepair was incomplete. In the present study, we validated if the senolytic cocktail dasatinib and quercetin (D+Q) could reboot the neurogenic output by clearing chronic senescent cells from the aged killifish brain to re-create the necessary supportive environment. Our results confirm that the aged killifish telencephalon holds a very high senescent cell burden, which we could diminish by short-term systemic D+Q treatment. As a consequence of D+Q administration, proliferation of non-glial progenitors increased and more new neurons were generated and migrated into the parenchyma after injury. Injury-induced inflammation and glial scarring, a phenomenon only seen in aged killifish, remained unaltered. Senolytic treatment with D+Q might thus hold promise for improving brain function in aged populations, and is especially interesting for reviving the neurogenic potential of an already aged central nervous system.

2023-07-20 | PXD036437 | Pride

Rattus norvegicus

Project description:Traumatic brain injury

| PRJNA1065340 | ENA

giza-affy-rat-84719

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. Keywords: time-course

2005-07-06 | GSE2871 | 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

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