Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

KLF6 alleviates hepatic ischemia-reperfusion injury by inhibiting autophagy

ABSTRACT: KLF6 alleviates hepatic ischemia-reperfusion injury by inhibiting autophagy

PROVIDER: PRJNA894155 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

KLF6 alleviates hepatic ischemia-reperfusion injury by inhibiting autophagy

Project description:To find the genes with significant expression changes after liver ischemia-reperfusion injury,we established a hypoxia-reoxygenation model using AML12 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq under normoxia and hypoxia-reoxygenation conditions.

2022-10-30 | GSE216522 | GEO

KLF6 alleviates hepatic ischemia-reperfusion injury by inhibiting autophagy.

Project description:Hepatic ischemia-reperfusion (I/R) injury, a common clinical complication of liver transplantation, gravely affects patient prognosis. Krüppel-like factors (KLFs) constitute a family of C2/H2 zinc finger DNA-binding proteins. KLF6, a member of the KLF protein family, plays crucial roles in proliferation, metabolism, inflammation, and injury responses; however, its role in HIR is largely remains unknown. After I/R injury, we found that KLF6 expression in mice and hepatocytes was significantly upregulated. Mice were then subjected to I/R following injection of shKLF6- and KLF6-overexpressing adenovirus through the tail vein. KLF6 deficiency markedly exacerbated liver damage, cell apoptosis, and activation of hepatic inflammatory responses, whereas hepatic overexpression of KLF6 in mice produced the opposite results. In addition, we knocked out or overexpressed KLF6 in AML12 cells before exposing them to a hypoxia-reoxygenation challenge. KLF6 knockout decreased cell viability and increased hepatocyte inflammation, apoptosis, and ROS, whereas KLF6 overexpression had the opposite effects. Mechanistically, KLF6 inhibited the overactivation of autophagy at the initial stage, and the regulatory effect of KLF6 on I/R injury was autophagy-dependent. CHIP-qPCR and luciferase reporter gene assays confirmed that KLF6 bound to the promoter region of Beclin1 and inhibited its transcription. Additionally, KLF6 activated the mTOR/ULK1 pathway. Finally, we performed a retrospective analysis of the clinical data of liver transplantation patients and identified significant associations between KLF6 expression and liver function following liver transplantation. In conclusion, KLF6 inhibited the overactivation of autophagy via transcriptional regulation of Beclin1 and activation of the mTOR/ULK1 pathway, thereby protecting the liver from I/R injury. KLF6 is expected to serve as a biomarker for estimating the severity of I/R injury following liver transplantation.

| S-EPMC10313896 | biostudies-literature

Vitamin B12 alleviates myocardial ischemia/reperfusion injury

Project description:Vitamin B12 alleviates myocardial ischemia/reperfusion injury

| PRJNA933927 | ENA

Vitamin B12 alleviates myocardial ischemia/reperfusion injury

Project description:To examine the protective effect of B12 on myocardial ischemia/reperfusion injury and figure out the mechanism of B12.

2024-01-01 | GSE225105 | GEO

FGF18 alleviates hepatic ischemia-reperfusion injury via the USP16-mediated KEAP1/Nrf2 signaling pathway in male mice

Project description:Hepatic ischemia-reperfusion injury (IRI) is a common complication occurs during hepatic resection and transplantation. However, the mechanisms underlying hepatic IRI have not been fully elucidated. Here, we aim to explore the role of fibroblast growth factor 18 (FGF18) in hepatic IRI. In this work, we find that Hepatic stellate cells (HSCs) secrete FGF18 and alleviates hepatocytes injury. HSCs-specific FGF18 deletion largely aggravates hepatic IRI. Mechanistically, FGF18 treatment reduces the levels of ubiquitin carboxyl-terminal hydrolase 16 (USP16), leading to increased ubiquitination levels of Kelch Like ECH Associated Protein 1 (KEAP1) and the activation of nuclear factor erythroid 2-related factor 2 (Nrf2). Furthermore, USP16 interacts and deubiquitinates KEAP1. More importantly, Nrf2 directly binds to the promoter of USP16 and forms a negative feedback loop with USP16. Collectively, our results show FGF18 alleviates hepatic IRI by USP16/KEAP1/Nrf2 signaling pathway in male mice, suggesting that FGF18 represents a promising therapeutic approach for hepatic IRI.

2023-09-05 | GSE242032 | GEO

Differential expression of mRNAs in the heart of ischemia-reperfusion mice

Project description:To identify the role of mRNA during myocardial ischemia-reperfusion in mice, we have employed high-throughput sequencing to detect mRNA expression. Samples were collected from the control group and the ischemia reperfusion groups , with 5 samples per group. The candidate mRNA that may affect the process of myocardial ischemia-reperfusion was screened by comparing the ischemia-reperfusion group and the control group.

2023-11-15 | GSE223343 | GEO

Transcription profiling of rat NRVMs response to ischemia and reperfusion events using Coverslip Hypoxia

Project description:NRVMs were subjected to varying durations of ischemia or ischemia+reperfusion using coverslip hypoxia. Expression profiling was used to identify genes that are differentially regulated in either event. We used microarrays to detail the global program of gene expression underlying ischemia and reperfusion using Coverslip Hypoxia and identified distinct classes of genes regulated during these processes. Experiment Overall Design: RNA was extracted from NRVMs subjected to varying durations of ischemia or ischemia+reperfusion and hybridized to rat genome Affymetrix arrays.

2008-06-15 | E-GEOD-6701 | biostudies-arrayexpress

Mouse kidney ischemia-reperfusion injury time course

Project description:Time course experiments involving bilateral renal ischemia reperfusion injury (IRI) in C57BL/6J mice (0 hr control, 20 min bilateral ischemia without reperfusion, 4, 16, 24, 36, 48, and 72 hrs post IRI). This dataset also includes IRI at 48 hrs and 72 hrs in Azin1 A-to-I locked and Azin1 A-to-I uneditable mice.

2024-09-30 | GSE267650 | GEO

MicroRNA Profiling in Ischemia-Reperfusion Injury of the Gracilis Muscle in Rats

Project description:This SuperSeries is composed of the following subset Series: GSE21405: MicroRNA Profiling In Ischemia-Reperfusion Injury Of The Gracilis Muscle In Rats GSE21406: Potential Target Genes of MicroRNA-21 In Ischemia-Reperfusion Injury Of The Gracilis Muscle In Rats Refer to individual Series

2010-04-22 | E-GEOD-21423 | biostudies-arrayexpress

Pulmonary gene expression after ischemia reperfusion in young and old mice

Project description:To examine the age-related vulnerability to lung ischemia reperfusion injury, pulmonary gene expression profiles after lung ischemia reperfusion were compared between young and old mice.

2024-04-06 | GSE211951 | 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