Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Early brain microRNA and mRNA expression profiles after neonatal hypoxic-ischemic injury in a mouse model

ABSTRACT: Early brain microRNA and mRNA expression profiles after neonatal hypoxic-ischemic injury in a mouse model

PROVIDER: PRJNA767342 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16117800.fastq.gz	Fastqsanger.gz
	SRR16117801.fastq.gz	Fastqsanger.gz
	SRR16117802.fastq.gz	Fastqsanger.gz
	SRR16117803.fastq.gz	Fastqsanger.gz
	SRR16117804.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

Early brain microRNA and mRNA expression profiles after neonatal hypoxic-ischemic injury in a mouse model [NanoString]

Project description:We report the miRNA-Seq and Nanostring mRNA data from regional brain samples after neonatal hypoxic-ischemic brain injury (induced by unilateral carotid artery ligation and 30 minutes at 8% oxygen in CD1 mice at postnatal day 9). Analyses are perfomed in the cerebellum, striatum/thalamus, and whole cortex. Examination of regional small RNA expression between four postnatal day 9 mouse pups after hypoxic-ischemic brain injury versus four sham surgery controls

2021-10-01 | GSE184995 | GEO

Early brain microRNA and mRNA expression profiles after neonatal hypoxic-ischemic injury in a mouse model [miRNA-Seq]

2021-10-01 | GSE184939 | GEO

Early brain microRNA and mRNA expression profiles after neonatal hypoxic-ischemic injury in a mouse model [NanoString]

Project description:Early brain microRNA and mRNA expression profiles after neonatal hypoxic-ischemic injury in a mouse model [NanoString]

| PRJNA767347 | ENA

Early brain microRNA and mRNA expression profiles after neonatal hypoxic-ischemic injury in a mouse model [miRNA-Seq]

Project description:Early brain microRNA and mRNA expression profiles after neonatal hypoxic-ischemic injury in a mouse model [miRNA-Seq]

| PRJNA767344 | ENA

Comprehensive gene expression analysis of cerebral cortices from mature rats after neonatal hypoxic-ischemic brain injury

Project description:Neonatal hypoxic-ischemic (HI) encephalopathy can lead to severe brain damage and is a common cause of neurological handicaps in adulthood. To elucidate the molecular events occurring in cerebral cortices of mature rats (8 weeks old) after neonatal HI brain insult, we performed comprehensive gene expression and gene network analyses using a DNA microarray system (Agilent 4x44K). A rat model of neonatal HI encephalopathy (Rice model) was obtained by unilateral ligation of the common carotid artery of 7-day-old rats with hypoxia (exposure to 8% oxygen). Due to the HI insult-related breakdown of the ipsilateral hemisphere in the brain, RNAs were prepared from the contralateral cerebral cortices of 8-week-old rats and analyzed by DNA microarray. Biofunctional analysis of differentially regulated genes revealed that many upregulated genes were related to cell death signaling, such as the arachidonic acid cascade. In contrast, many downregulated genes were related to gene expression, reflecting progressive damage by the HI insult, even within the contralateral cerebral hemisphere. Seven-day-old Wistar rats were assigned to two groups: the control group and the Rice group (four pups in each group). HI brain insult was not induced in the control group rats. The Rice group rats were subjected to a modified LevineM-bM-^@M-^Ys procedure to induce HI brain injury. The Rice group rats were anesthetized with ether, and the left carotid artery was sectioned between double ligatures with 4-0 surgical silk. The rats were allowed to recover for 1M-bM-^@M-^S2 h and then exposed to 1 h of hypoxia in a plastic chamber that was perfused with a mixture of humidified 8% oxygen balanced with nitrogen. The temperature inside the chamber was maintained at 33 M-BM-0C, the usual temperature generated when pups huddle with the mother. The cerebral cortexes contralateral to the HI brain insult and those of the same side of the control animals were used for the experiment.

2012-06-27 | E-GEOD-37777 | biostudies-arrayexpress

Echinatin alleviates inflammation and pyroptosis in hypoxic-ischemic brain damage by inhibiting TLR4/ NF-κB pathway

Project description:Hypoxic ischemic encephalopathy (HIE) is a primary cause of neonatal death and disabilities resulting from perinatal hypoxia. The progression of HI injury is closely associated with neuroinflammation. Therefore, suppressing inflammatory pathways is a promising therapeutic strategy for treating HIE. Echinatin (Ech) is a principal active component of glycyrrhiza, with anti-inflammatory and anti-oxidative effects, often combined with other herbs to exert effects of clearing heat and detoxifying. This study aimed to investigate the anti-inflammatory and neuroprotective effects of Ech on neonatal rats with hypoxic-ischemic brain damage and on PC12 cells induced by oxygen-glucose deprivation (OGD).

2024-05-07 | GSE266886 | GEO

Sodium Butyrate(SB) mediates Histone Crotonylation and Alleviated Neonatal Rats Hypoxic -Ischemic Brain Injury Through Gut-Brain Axis [ChIP-seq]

Project description:Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf, and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.

2022-09-27 | GSE205142 | GEO

Genome-wide alteration of 5-hydroxymethylcytosine in hypoxic-ischemic neonatal rat model of cerebral palsy

Project description:Our results revealed that hypoxic-ischemic brain injury decreased the overall 5hmC abundance in rat temporal cortex, and these results suggest that 5hmC modifications are involved in the cerebral palsy pathogenesis.

2019-07-04 | GSE133787 | GEO

Comprehensive gene expression analysis of cerebral cortices from mature rats after neonatal hypoxic-ischemic brain injury

2012-06-28 | GSE37777 | GEO

Sodium Butyrate mediates Histone Crotonylation and Alleviated Neonatal Rats Hypoxic -Ischemic Brain Injury Through Gut-Brain Axis [RNA-seq]

Project description:CurrentNeonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf, and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.

2022-09-27 | GSE205143 | 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