Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of traumatic brain injury on gene expression in bone.

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE253133 | GEO | 2024/01/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome profiling in the DA and PVG inbred rat strains after traumatic brain injury

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

Traumatic Brain Injury Stimulates Sympathetic Tone-mediated Bone Marrow Myelopoiesis to Favor Fracture Healing

Project description:Traumatic brain injury (TBI) accelerates fracture healing, but the underlying mechanism remains largely unknown. Accumulating evidence indicates that the central nervous system plays a pivotal role in regulating immune system and skeleton, however, the impact of TBI on hematopoiesis commitment was overlooked. Here, we found that the dramatically elevated sympathetic tone accompanied with TBI-accelerated fracture healing; chemical sympathectomy blocks TBI-induced fracture healing. Importantly, the adrenergic hypersensitivity swiftly skews bone marrow hematopoietic lineage cells toward anti-inflammation myeloid cells within 14 days, which favor fracture healing. Knockout of β3- or β2-adrenergic receptors (ARs) eliminate TBI mediated anti-inflammation macrophage expansion and TBI-accelerated fracture healing. Moreover, β3- and β2-ARs agonists synergistically promote M2 macrophages infiltration in callus and accelerate bone healing process. Our results suggest that TBI shapes the anti-inflammation environment during early stage of fracture healing, implicating the sympathetic nerve system as a potential target that can be exploited to treat fracture.

2023-04-12 | GSE229258 | GEO

Gene expression profiles after traumatic brain injury

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

The dentate gyrus after traumatic brain injury [miRNA]

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

The dentate gyrus after traumatic brain injury [mRNA]

Project description:Analysis of the dentate gyrus of traumatic brain injury model. Results provide insight into the molecular mechanism underlying TBI.

2017-02-25 | GSE86579 | GEO

Chronic Gene Expression after Traumatic Brain Injury

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

Integrated single-cell multiomics reveals novel immune candidate markers for post-traumatic coagulopathy

Project description:Introduction: Post-traumatic coagulopathy (PTC) is a critical pathology in traumatic brain injury (TBI), however, its potential mechanism is not clear. To explore this in peripheral samples, we integrated single cell RNA-sequencing and T cell repertoire (TCR)-sequencing across a cohort of patients with TBI. Methods: Clinical samples from patients with more brain severity demonstrated altered mRNAs.

2023-02-02 | GSE223245 | GEO

Targeting pyroptosis with nanoparticles to alleviate neuroinflammatory for preventing secondary damage following traumatic brain injury

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

Proteomic analysis identifies plasma correlates of remote ischemic conditioning in the context of experimental traumatic brain injury

Project description:Remote ischemic conditioning (RIC) treatment has been shown to modify levels of traumatic brain injury (TBI) pathology related proteins, however, the mechanism is not widely understood. This study utilized LC-MS/MS to identify protein biomarkers of RIC treatment after TBI in mouse models.

2021-06-03 | PXD020420 | Pride

Microglia adopt longitudinal transcriptional changes after traumatic brain injury

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data