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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

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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

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [ChIP-Seq]

Project description:We performed ChIP-seq to find the trageted genes regulated by ATF3 in hypoxia/reoxygenation (H/R)using ATF3 antibody for ChIP.

2023-01-01 | GSE193996 | GEO

Down-regulation of NDRG1 promotes migration of cancer cells during reoxygenation

2012-01-01 | GSE30019 | GEO

Down-regulation of NDRG1 promotes migration of cancer cells during reoxygenation

Project description:To investigate the transcriptional response of tumor adaptation to reoxygenation, breast cancer cells MCF-7 was cultured under 0.5% of hypoxia for 24h followed by 24h of reoxygenation in normoxia. Cells were harvested respectively at 0, 1, 4, 8, 12, and 24h during reoxygenation. Total RNA obtained from human breast cancer cell line MCF-7 were collected respectively at 0, 1, 4, 8, 12 and 24 hours after reoxygenation.

2012-01-01 | E-GEOD-30019 | biostudies-arrayexpress

Ischemic Postconditioning Alleviates Cerebral Ischemia-Reperfusion Injury Through Activating Autophagy During Early Reperfusion in Rats.

Project description:This study aimed to investigate whether ischemic postconditioning (IpostC) alleviates cerebral ischemia/reperfusion (I/R) injury involved in autophagy. Adult Sprague-Dawley rats were divided into five groups: sham (sham surgery), I/R (middle cerebral artery occlusion [MCAO] for 100 min, then reperfusion), IpostC (MCAO for 100 min, reperfusion for 10 min, MCAO for 10 min, then reperfusion), IpostC+3MA (3-methyladenine, an autophagy inhibitor, administered 30 min before first reperfusion), and IpostC+Veh (vehicle control for IpostC+3MA group). Infarct volume was measured using cresyl violet staining. Autophagy-related proteins were detected by western blot and immunohistochemistry. Autophagosomes, autophagolysosomes, and mitochondrial damage were identified by transmission electron microscopy. Cortical cell apoptosis was detected by the TUNEL assay. Neurologic function was assessed using the modified Neurologic Severity Score. IpostC improved neurological function and reduced infarct volume after I/R (P?<?0.05). These effects of IpostC were inhibited by 3MA (P?<?0.05). Autophagosome formation was increased in the I/R and IpostC+Veh groups (P?<?0.05), but not in the IpostC+3MA group. The I/R group showed enhanced LC3-II/LC3-I ratio, p62, and Cathepsin B levels and decreased LAMP-2 level (all P?<?0.05 vs. sham), indicating dysfunction of autophagic clearance. IpostC reduced p62 and Cathepsin B levels and increased the LC3-II/LC3-I ratio, and nuclear translocation of transcription factor EB (all P?<?0.05); these effects of IpostC were reversed by 3MA, suggesting IpostC enhanced autophagic flux. Furthermore, IpostC attenuated I/R-induced mitochondrial translocation of Bax and mitochondrial cytochrome-c release (all P?<?0.05); 3MA inhibited these effects of IpostC (P?<?0.05). In conclusion, IpostC may alleviate cerebral I/R injury by activating autophagy during early reperfusion.

| S-EPMC6096887 | biostudies-other

OL-FS13 Alleviates Cerebral Ischemia-reperfusion Injury by Inhibiting miR-21-3p Expression.

Project description:BackgroundOL-FS13, a neuroprotective peptide derived from Odorrana livida, can alleviate cerebral ischemia-reperfusion (CI/R) injury, although the specific underlying mechanism remains to be further explored.ObjectiveThe effect of miR-21-3p on the neural-protective effects of OL-FS13 was examined.MethodsIn this study, the multiple genome sequencing analysis, double luciferase experiment, RT-qPCR, and Western blotting were used to explore the mechanism of OL-FS13.ResultsShowed that over-expression of miR-21-3p against the protective effects of OL-FS13 on oxygen- glucose deprivation/re-oxygenation (OGD/R)-damaged pheochromocytoma (PC12) cells and in CI/R-injured rats. miR-21-3p was then found to target calcium/calmodulin-dependent protein kinase 2 (CAMKK2), and its overexpression inhibited the expression of CAMKK2 and phosphorylation of its downstream adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK), thereby inhibiting the therapeutic effects of OL-FS13 on OGD/R and CI/R. Inhibition of CAMKK2 also antagonized up-regulated of nuclear factor erythroid 2-related factor 2 (Nrf-2) by OL-FS13, thereby abolishing the antioxidant activity of the peptide.ConclusionOur results showed that OL-FS13 alleviated OGD/R and CI/R by inhibiting miR-21-3p to activate the CAMKK2/AMPK/Nrf-2 axis.

| S-EPMC10616927 | biostudies-literature

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 2]

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived neonatal mouse cells' transcriptome profiling (RNA-seq) to microarray method and to evaluate protocols for optimal high-throughput data analysis, to find the trageted genes regulated by ATF3 in Hypoxia/Reoxygenation(H/R)

2023-01-01 | GSE193999 | GEO

Emodin alleviates myocardial ischemia/reperfusion injury by inhibiting gasdermin D-mediated pyroptosis in cardiomyocytes.

Project description:BackgroundEmodin has recently been reported to have a powerful antiinflammatory effect, protecting the myocardium against ischemia/reperfusion (I/R) injury. Pyroptosis is a proinflammatory programmed cell death that is related to many diseases. The present study investigated the effect of emodin on pyroptosis in cardiomyocytes.Materials and methodsSprague Dawley rats were randomly divided into sham, I/R, and I/R+Emodin groups. I/R model was subjected to 30 minutes' ligation of left anterior descending coronary artery, followed by 2 hours of reperfusion. Cardiomyocytes were exposed to hypoxic conditions for 1 hour and normoxic conditions for 2 hours. The level of the pyroptosis was detected by Western blot, real-time PCR analysis, and ELISA.ResultsThe level of gasdermin D-N domains was upregulated in cardiomyocytes during I/R or hypoxia/reoxygenation (H/R) treatment. Moreover, emodin increased the rate of cell survival in vitro and decreased the myocardial infarct size in vivo via suppressing the levels of I/R-induced pyroptosis. Additionally, the expression of TLR4, MyD88, phospho-IκBα, phospho-NF-κB, and the NLRP3 inflammasome was significantly upregulated in cardiomyocytes subjected to H/R treatment, while emodin suppressed the expression of these proteins.ConclusionThis study confirms that emodin treatment was able to alleviate myocardial I/R injury and inhibit pyroptosis in vivo and in vitro. The inhibitory effect of emodin on pyroptosis was mediated by suppressing the TLR4/MyD88/NF-κB/NLRP3 inflammasome pathway. Therefore, emodin may provide an alternative treatment for myocardial I/R injury.

| S-EPMC6438141 | biostudies-literature

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

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