Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron

ABSTRACT: MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron

PROVIDER: PRJNA340071 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Rattus norvegicus

Project description:MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron [mRNA]

| PRJNA340072 | ENA

Rattus norvegicus

Project description:MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron [miRNA]

| PRJNA340073 | ENA

MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-08-26 | GSE86034 | GEO

MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron [mRNA]

Project description:Comparison of the differential expression mRNA profiles from the brain cortex of hypoxia and normaixa rats by silica microarray chip

2016-08-26 | GSE85825 | GEO

MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron [miRNA]

Project description:Comparison of the differential expression mRNA profiles from the brain cortex of hypoxia and normaixa rats by silica microarray chip.

2016-08-26 | GSE86033 | GEO

The miR-92a–Cpeb3 axis safeguards neuronal function during neuroinflammation

Project description:Neuroinflammation causes neuronal injury in multiple sclerosis (MS) and other neurological diseases. MicroRNAs (miRNAs) are central modulators of cellular stress responses, but knowledge about miRNA–mRNA interactions that determine neuronal outcome during inflammation is limited. Here, we combined unbiased neuron-specific miRNA with mRNA sequencing to assemble the regulatory network that mediates robustness against neuroinflammation. As a critical miRNA-network hub we defined miR-92a. Genetic deletion of miR-92a exacerbated the disease course of mice undergoing experimental autoimmune encephalomyelitis (EAE), whereas miR-92a overexpression protected neurons against excitotoxicity. As a key miR-92a target transcript, we identified cytoplasmic polyadenylation element-binding protein 3 (Cpeb3) that was suppressed in inflamed neurons in mouse EAE and human MS. Accordingly, Cpeb3 deletion improved neuronal resistance to excitotoxicity and ameliorated EAE. Together, we discovered that the miR-92a–Cpeb3 axis confers neuronal robustness against inflammation and serves as potential target for neuroprotective therapies.

2023-11-06 | GSE220950 | GEO

Pisolithus sp. 92A

Project description:Pisolithus sp. 92A Resequencing

| PRJNA444305 | ENA

Fumaric acid esters can block pro-inflammatory actions of human CRP and ameliorate metabolic disturbances in transgenic spontaneously hypertensive rats

Project description:Inflammation and oxidative stress have been implicated in the pathogenesis of metabolic disturbances. Esters of fumaric acid, mainly dimethyl fumarate (DMF), exhibit immunomodulatory, anti-inflammatory, and anti-oxidative effects. In the current study, we tested the hypothesis that fumaric acid ester treatment of an animal model of inflammation and metabolic syndrome, the spontaneously hypertensive rat transgenically expressing human C-reactive protein (SHR-CRP), will ameliorate inflammation, oxidative stress, and metabolic disturbances.

2015-12-31 | E-MTAB-2406 | biostudies-arrayexpress

Genes downregulated by miR-92a-1-5p overexpression in K562 cells treated with imatinib.

Project description:In order to indetify new target genes of miR-92a-1-5p in chronic myeloid leukemia, K562 cells carrying the BCR::ABL1 fusion gene were transiently transfected with miR-92a mimic or scramble and treated with imatinib. RNA was sequenced to identify genes expressed under imatinib treatment and downregulated after miR-92a-1-5p overexpression.

2024-10-11 | GSE278906 | GEO

Exosomal miR-92a-3p as a diagnostic biomarker for adenomyosis and its pathological mechanism

Project description:This study aimed to elucidate the role of microRNA miR-92a-3p in the pathogenesis of adenomyosis. We focused on understanding how miR-92a-3p in exosomes derived from ectopic lesions influences the behavior of endometrial cells, DRG neurons, and Human Umbilical Vein Endothelial Cells (HUVECs), and its potential as a non-invasive diagnostic biomarker. Our findings revealed that MiR-92a-3p is significantly upregulated in exosomes derived from ectopic lesions of adenomyosis. This upregulation was associated with enhanced migration and invasion capabilities in eutopic endometrial cells, DRG neurons, and HUVECs. Furthermore, the study demonstrated a significant correlation between the levels of MiR-92a-3p in urinary exosomes and the clinical symptoms of adenomyosis, suggesting its potential as a non-invasive biomarker for the disease. This study elucidates an exosomal signaling process via miR-92a-3p that drives pathological infiltration and angiogenesis to promote adenomyosis progression. Upregulated miR-92a-3p in biofluid exosomes shows promising non-invasive biomarker potential for diagnosis and monitoring of this disease. Our findings unveil novel targets and tools for improved clinical management.

2024-04-01 | GSE262302 | 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