Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic Analysis of Rat Cerebral Cortex Reveals the Potential Mechanism of Electroacupuncture Opening Blood Brain Barrier

ABSTRACT: Transcriptomic Analysis of Rat Cerebral Cortex Reveals the Potential Mechanism of Electroacupuncture Opening Blood Brain Barrier

PROVIDER: PRJNA793677 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17400880_1.fastq.gz	Fastqsanger.gz
	SRR17400880_2.fastq.gz	Fastqsanger.gz
	SRR17400881_1.fastq.gz	Fastqsanger.gz
	SRR17400881_2.fastq.gz	Fastqsanger.gz
	SRR17400882_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Transcriptomic Analysis of Rat Cerebral Cortex Reveals the Potential Mechanism of Electroacupuncture Opening Blood Brain Barrier

2022-01-05 | GSE192885 | GEO

Profiling the rat cortical single-cell transcriptome reveals the potential mechanism of specific mode electroacupuncture stimulation opening the blood-brain barrier

Project description:The existence of the blood-brain barrier (BBB) dramatically limits the drug treatment of central nervous system diseases such as stroke, neurodegenerative diseases, and brain tumors. Due to the complexity of the structure and function of the blood-brain barrier, it has been challenging to develop central nervous system drug delivery strategies and reveal critical biological mechanisms. Our previous studies have confirmed that specific mode electroacupuncture stimulation (EA) can effectively open the BBB in rats. Here, we utilized single-cell RNA sequencing (scRNA-seq) to map the cell population of rat cerebral cortex comprehensively. We identified 23 cell subsets and 8 types of cells in the brain obtained by cell annotation, and explored the potential mechanism of EA to open the blood-brain barrier by bioinformatics analysis of specific cell subsets and cell types, as well as cell communications. In summary, scRNA-seq uncovers the transcriptional changes of the cerebral cortex under EA at the single cell level; our results provide rich insights into the molecular and cellular architecture changes of the brain after EA intervention and provide a new reference for BBB material transport and its drug delivery research in health and disease, providing new potential strategies into the mechanism of BBB opening and provide essential information for designing rational treatment regimens and optimizing drug delivery.

2024-07-24 | GSE272895 | GEO

Albumin, TGF-Beta1 and Blood-Brain Barrier opening induce cortical epileptogenesis.

Project description:Insults to the cerebral cortex, such as trauma, ischemia or infections, may result in the development of epilepsy, one of the most common neurological disorders. Previous studies have suggested that perturbations in neurovascular integrity and breakdown of the blood-brain barrier (BBB) lead to neuronal hypersynchronization and epileptiform activity, but the underlying mechanisms are unknown. As with BBB opening, treatment with albumin or with TGF-?1 results in the development of hypersynchronized epileptiform activity. Given the latent period before the appearance of epileptiform activity, we hypothesized the underlying mechanism is a transcriptional response which would be similar for BBB breakdown and exposure to albumin or TGF-?1. In search of a common pathway and transcriptional activation pattern we performed a genome wide analysis. Genomic expression analyses demonstrated similar expression patterns for BBB opening, albumin and TGF-?1 exposure. Most importantly, TGF-? pathway blockers suppressed most albumin-induced transcriptional changes. RNA was extracted from cortical regions of rats treated with sodium deoxycholate (DOC, to induce BBB opening), albumin or TGF-?1 for various durations (7/8, 24, 48hr). Control RNA was extracted from a sham-operated animal and one array was run for each treatment and time point A second set of animals (labeled as Set 2) was treated with either albumin (n=3) or albumin in the presence of TGF-? receptor blockers (n=4; TGF-?R1 kinase activity inhibitor SB431542 and TGF-?R2 antibody) and sacrificed 24 hr following treatment. Sham-operated animals served as controls (n=2).

2009-07-15 | E-GEOD-12304 | biostudies-arrayexpress

Transcriptome profiling of mRNAs in cortex of normal rats with electroacupuncture

Project description:We analyzed transcriptomic characteristic of motor cortex from Sprague-Dawley rat brain treated with electroacupuncture.

2024-01-12 | GSE222706 | GEO

Albumin, TGF-Beta1 and Blood-Brain Barrier opening induce cortical epileptogenesis.

2009-07-15 | GSE12304 | GEO

RNA-seq of mouse primary somatosensory cortex (S1) in a neuropathic pain model after electroacupuncture stimulus

Project description:This study aims to identify the molecular mechanism in the sensory cortex underlying pain-relief effect of electroacupuncture

2021-01-09 | E-MTAB-9987 | biostudies-arrayexpress

Transcriptomic Analysis of Rat Cerebral Cortex Reveals the Potential Mechanism of Electroacupuncture Opening Blood Brain Barrier.

Project description:Therapeutic treatment options for central nervous system (CNS) diseases are greatly limited by the blood-brain barrier (BBB). Electroacupuncture (EA) can be used to induce an increase in BBB permeability on rats, providing a potential approach for the delivery of drugs from the systemic circulation into the brain. However, there remains a large gap in our knowledge regarding the impact of EA on brain gene expression. This work is focused on investigating the transcriptional changes of rat cerebral cortex following EA and expression changes in genes and bioinformatic analysis was performed. We found that the potential mechanism of EA opening BBB involves receptor-mediated/carrier-mediated endocytosis (RMT/CMT), and related genes include solute carrier (SLC) transporter genes and ATP-binding cassette (ABC) transporter genes. The results also suggested that EA may affect the expression of tight junction (TJ) proteins in endothelial cells by affecting integrin binding, autophagy pathway and calcium signaling pathway, thus further affecting the permeability of blood-brain barrier. Our results provide a valuable resource that will guide mechanism research of EA opening BBB and other ways to mediate drug delivery into the brain.

| S-EPMC8908321 | biostudies-literature

Expression data from mouse cerebral cortex

Project description:Differential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains We used Affymetrix microarray to explore the global gene expression patterns of mouse cerebral cortex of different mouse strains at two developmental stages Cerebral cortex from two mouse strains [C57BL/6J(B6) and C3H/J (C3H)] at post-natal day 1 (p1) and post-natal 11 weeks (11 wk) were harvested for microarray experiments

2013-10-21 | E-GEOD-46443 | biostudies-arrayexpress

Exploring the effect of electroacupuncture stimulation of Lung Meridian of Hand-Taiyin on synaptic plasticity in rats with cerebral ischemia-reperfusion injury based on Transcriptomics

Project description:Background: Electroacupuncture (EA) were progressively gained popularity in the treatment of neurological disorders such as ischaemic brain injury in recent years. But the therapeutic mechanisms of EA are yet not well addressed. This research aims to explore the effect of electroacupuncture stimulation of Lung Meridian of Hand-Taiyin on synaptic plasticity in rats with cerebral ischemia-reperfusion injury based on Transcriptomics Methods: Rats were randomly divided into sham operation group, model group and EA group. Rats in the model group and the EA group were prepared for the middle cerebral artery occlusion/reperfusion (MCAO/R) model. In the EA group, the representative acupoints of the Lung Meridian of Hand-Taiyin (Tianfu acupoints, Chize acupoints, Kongzui acupoints and Taiyuan acupoints) were selected for electroacupuncture stimulation. Transcriptomics was performed after the intervention.

2022-10-13 | GSE211253 | GEO

Metabolomic signature of mouse cerebral cortex following Toxoplasma gondii infection

Project description:BACKGROUND: The protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. However, the molecules that contribute to these changes remain largely unknown.METHODS: We have investigated the impact of T. gondii infection on the overall metabolism of mouse cerebral cortex. Mass-spectrometry-based metabolomics and multivariate statistical analysis were employed to discover metabolomic signatures that discriminate between cerebral cortex of T. gondii-infected and uninfected control mice.RESULTS: Our results identified 73, 67 and 276 differentially abundant metabolites, which were involved in 25, 37 and 64 pathways at 7, 14 and 21 days post-infection (dpi), respectively. Metabolites in the unsaturated fatty acid biosynthesis pathway were upregulated as the infection progressed, indicating that T. gondii induces the biosynthesis of unsaturated fatty acids to promote its own growth and survival. Some of the downregulated metabolites were related to pathways, such as steroid hormone biosynthesis and arachidonic acid metabolism. Nine metabolites were identified as T. gondii responsive metabolites, namely galactosylsphingosine, arachidonic acid, LysoSM(d18:1), L-palmitoylcarnitine, calcitetrol, 27-Deoxy-5b-cyprinol, L-homophenylalanine, oleic acid and ceramide (d18:1/16:0).CONCLUSIONS: Our data provide novel insight into the dysregulation of the metabolism of the mouse cerebral cortex during T. gondii infection and have important implications for studies of T. gondii pathogenesis.

2020-04-23 | MTBLS770 | MetaboLights

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