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: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE216522 | GEO | 2022/10/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

KLF6 alleviates hepatic ischemia-reperfusion injury by inhibiting autophagy

Project description:KLF6 alleviates hepatic ischemia-reperfusion injury by inhibiting autophagy

| PRJNA894155 | 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

Gallic Acid Pretreatment Mitigates Parathyroid Ischemia-Reperfusion Injury through Signaling Pathway Modulation

Project description:As a polyphenolic herbal extract, Gallic acid (GA) is known for its antioxidant and anti-inflammatory properties. However, its application in parathyroid ischemia-reperfusion injury (IRI) has not been well examined. This study aimed to elucidate the protective effects of GA pretreatment in a parathyroid IRI model and explore the underlying mechanisms.Hypoxia and hypoxia/reoxygenation models were established with primary parathyroid cells to explore the protective effect of GA.The results from sequencing and bioinformatic analyses indicated that GA might regulate MMP1, MMP9, FOSB, GSY2, DUSP5, TRPV1/3, TIAM1 and multiple signaling pathways in this process such as IL-17, AMPK, MAPK, Transient Receptor Potential (TRP) channels, cAMP and Rap1.

2023-08-23 | GSE240162 | 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

Proteomics analysis of human intestinal organoids during hypoxia and reoxygenation as a model to study ischemia-reperfusion injury

Project description:Intestinal ischemia-reperfusion (IR) injury is associated with high mortality rates, which have not improved in the past decades despite advanced insight in its pathophysiology using in vivo animal and human models. The inability to translate previous findings to effective therapies emphasizes the need for a physiologically relevant in vitro model to thoroughly investigate mechanisms of IR-induced epithelial injury and test potential therapies. In this study, we demonstrate the use of human small intestinal organoids to model IR injury by exposing organoids to hypoxia and reoxygenation (HR). A mass-spectrometry-based proteomics approach was applied to characterize organoid differentiation and decipher protein dynamics and molecular mechanisms of IR injury in crypt-like and villus-like human intestinal organoids.

2021-01-11 | PXD022999 | Pride

Expression data in Ischemia and Reperfusion during microsurgical tissue transfer

Project description:Gene Expression of muscle tissue during microsurgical free tissue transfer was basicly studied in animal models. There was found activation of inflammatory and apoptotic cascades and of genes regulating intracellular metabolism. We used microarrays to detail the programme of gene expression in human muscle tissue which is activated during this process. Human muscle which was harvested during microsurgical free tissue transfer was used for RNA extraction and hybridization on Affymetrix microarrays. Muscle samples of the flap were taken during normoxia (I) after ischemia (II) and after reperfusion (III). Ischemia startet after dissecting the sustentative vessel. Reperfusion began after reanastomosing the vessel and restoring the blood supply.

2010-07-07 | E-GEOD-22761 | biostudies-arrayexpress

Expression data from ischemia and reperfusion events in NRVMs using Coverslip Hypoxia

2007-01-11 | GSE6701 | GEO

Hif2a-cardiomyocyte deficient mice response to myocardial ischemia and reperfusion

Project description:Analysis of heart of Hypoxia-inducible 2 alpha-deficient mice, specific in cardiomyocytes (Hif2aloxP/loxP Myosin Cre+) subjected to myocardial ishcemia reperfusion. Hif2a belongs to the family of transcription factors, that regulate a transcriptional response to tissue hypoxia.

2016-12-31 | GSE67308 | GEO

Vitamin B12 alleviates myocardial ischemia/reperfusion injury

Project description:Vitamin B12 alleviates myocardial ischemia/reperfusion injury

| PRJNA933927 | ENA