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Next Generation Sequencing Facilitates Quantitative Analysis of ischemic postconditioning (IPO) to attenuate hepatic ischemia-reperfusion injury in mice

ABSTRACT: This is the first study to investigate mRNA expression profiling in regard to hepatic I/R and IPO by next-generation RNA-Seq. Our results may provide an experimental basis for elucidating the underlying mechanism of IPO and reveal candidate biomarkers with which to assess hepatic I/R injury

ORGANISM(S): Mus musculus

PROVIDER: GSE117066 | GEO | 2019/02/13

REPOSITORIES: GEO

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circRNAs microarray analysis of ischemic postconditioning (IPO) to attenuate hepatic ischemia-reperfusion injury in mice

Project description:this is the first study to investigate circRNA expression profiling in regard to hepatic I/R and IPO by microarray analysis. Our results may provide an experimental basis for elucidating the underlying mechanism of IPO and reveal candidate biomarkers with which to assess hepatic I/R injury

2019-02-05 | GSE117524 | GEO

Ischemic Pre- and Post Conditioning has pronounced effects on Gene Expression Profiles in the Rat Liver after Ischemia/Reperfusion

Project description:Ischemia/reperfusion injuries is a known complication to hepatic surgery. Ischemic pre- (IPC) and postconditioning (IPO) protects the liver against ischemia/reperfusion-injuries. Expression profiling were performed on liver biopsies seeking to identify molecular mediators of the protective properties. 48 rats were divided into 5 groups; sham (n=8), IRI (n=10), IPC (n=10), IPO (n=10) and IPC+IPO (n=10). All rats except sham rats were subjected to 30 min of total liver ischemia and 30 min of reperfusion before liver biopsies were sampled. In the IPC group, liver ischemia was preceded by 10 min of hepatic ischemia, followed by 10 min of reperfusion. IPO were performed by three cycles of 30 sec of reperfusion and 30 sec of ischemia, applied immediately after the 30 min of total liver ischemia. In the IPC+IPO group the two interventions were combined.

2011-09-30 | E-GEOD-24430 | biostudies-arrayexpress

circRNAs microarray analysis of ischemic postconditioning (IPO) to attenuate hepatic ischemia-reperfusion injury in mice

Project description:circRNAs microarray analysis of ischemic postconditioning (IPO) to attenuate hepatic ischemia-reperfusion injury in mice

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Comprehensive circRNA expression profile during ischemic postconditioning attenuating hepatic ischemia/reperfusion injury.

Project description:Ischemic postconditioning (IPO) attenuates hepatic ischemia/reperfusion (I/R) injury. The aim of this study was to explore the role of circular RNAs (circRNAs) in the protective mechanism of IPO. In this study, microarray hybridization analysis was performed to determine the circRNA expression profile. Briefly, a total of 1599 dysregulated circRNAs were detected. The competitive endogenous RNA (ceRNA) network, including 6 circRNAs, 47 miRNAs and 90 mRNAs, indicated that the potential "housekeeping" function of circRNAs is dysregulated in hepatic I/R injury. Based on the validation results of selected circRNAs, miRNAs and mRNAs following qRT-PCR amplification, the mmu_circRNA_005186-miR-124-3p-Epha2 pathway was constructed. Dual-luciferase reporter analysis showed that miR-124-3p interacted directly with mmu_circRNA_005186 and Epha2 through the predicted binding sites, which suggested that mmu_circRNA_005186, serving as a miRNA sponge for miR-124-3p, regulated the expression of Epha2. Functionally, we explored the mechanism of mmu_circRNA_005186 in LPS-treated RAW264.7 cells which simulated the inflammation in hepatic I/R injury. We found that mmu_circRNA_005186 silencing attenuated the LPS-induced inflammation and was associated with miR-124-3p upregulation and Epha2 downregulation. Our study is the first to show that circRNAs are closely related to hepatic I/R injury and IPO and suggests that targeting mmu_circRNA_005186-miR-124-3p-Epha2 pathway might attenuate hepatic I/R injury.

| S-EPMC6342922 | biostudies-literature

Next Generation Sequencing Facilitates Quantitative Analysis of ischemic postconditioning (IPO) to attenuate hepatic ischemia-reperfusion injury in mice

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of ischemic postconditioning (IPO) to attenuate hepatic ischemia-reperfusion injury in mice

| PRJNA481000 | ENA

Ischemic Pre- and Post Conditioning has pronounced effects on Gene Expression Profiles in the Rat Liver after Ischemia/Reperfusion

2011-10-01 | GSE24430 | GEO

Ischemic postconditioning protects cardiomyocytes against ischemia/reperfusion injury by inducing MIP2.

Project description:Cardiomyocytes can resist ischemia/reperfusion (I/R) injury through ischemic postconditioning (IPoC) which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40 family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models, an in vivo open chest rat coronary artery occlusion model and an in vitro model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration) followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion, MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the in vitro model. These effects were blunted by transfection with MIP2 siRNA in the H9c2 cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.

| S-EPMC3174377 | biostudies-literature

Circular RNA microarray analyses in hepatic ischemia-reperfusion injury with ischemic preconditioning prevention

Project description:The study for the first time systematically detect the dysregulated circRNAs and mRNAs in response to hepatic IRI and IPC intervention. Our profile and bioinformatic analysis provide numerous of novel clews on the understanding the pathophysiologic mechanism of IPC protection against hepatic IRI.

2021-02-28 | GSE164367 | GEO

To Protect Fatty Livers from Ischemia Reperfusion Injury: Role of Ischemic Postconditioning.

Project description:BackgroundThe benefit of ischemic postconditioning (IPostC) might be the throttled inflow following cold ischemia. The current study investigated advantage and mechanisms of IPostC in healthy and fatty rat livers.MethodsMale SD rats received a high-fat diet to induce fatty livers. Isolated liver perfusion was performed after 24 h ischemia at 4 °C as well as in vivo experiments after 90 min warm ischemia. The so-called follow-up perfusions served to investigate the hypothesis that medium from IPostC experiments is less harmful. Lactate dehydrogenase (LDH), transaminases, different cytokines, and gene expressions, respectively, were measured.ResultsFatty livers showed histologically mild inflammation and moderate to severe fat storage. IPostC reduced LDH and TXB2 in healthy and fatty livers and increased bile flow. LDH, TNF-α, and IL-6 levels in serum decreased after warm ischemia + IPostC. The gene expressions of Tnf, IL-6, Ccl2, and Ripk3 were downregulated in vivo after IPostC.ConclusionsIPostC showed protective effects after ischemia in situ and in vivo in healthy and fatty livers. Restricted cyclic inflow was an important mechanism and further suggested involvement of necroptosis. IPostC represents a promising and easy intervention to improve outcomes after transplantation.

| S-EPMC7990852 | biostudies-literature

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

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