Circular RNA microarray analyses in hepatic ischemia-reperfusion injury with ischemic preconditioning prevention
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE164367 | GEO | 2021/02/28
REPOSITORIES: GEO
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Project description:We examined, through an oligonucleotide microarray protocol, the renal differential transcriptome profiles of mices submitted to IRI, IPC and Hemin treatment. After identifying the profiles of differentially expressed genes observed for each comparison, we carried out functional enrichment analysis to reveal transcripts putatively involved in potential relevant biological processes and signaling pathways. The most relevant enriched biological processes found in these comparisons were stress, inflammation, apoptosis, pathways in cancer, differentiation, angiogenesis, focal adhesion, ECM-receptor interaction, ion transport, angiogenesis, mitosis and cell cycle, inflammatory response, olfactory transduction and regulation of actin cytoskeleton. In addition, the most important overrepresented pathways were MAPK, ErbB, JAK/STAT, Toll and Nod like receptors, Angiotensin II, Arachidonic acid metabolism, Wnt and coagulation cascade. Also, new insights were gained about the underlying protection mechanisms against renal IRI promoted by IPC and Hemin treatment. Venn diagram analysis allowed us to uncover common and exclusively differentially expressed genes between these two protective maneuvers, underscoring potential common and exclusive biological functions regulated in each case. In summary, IPC exclusively regulated the expression of genes belonging to stress, protein modification and apoptosis, highlighting the role of IPC in controlling exacerbated stress response. Treatment with the Hmox1 inducer Hemin, in turn, exclusively regulated the expression of genes associated with cell differentiation, metabolic pathways, cell cycle, mitosis, development, regulation of actin cytoskeleton and arachidonic acid metabolism, suggesting a pleiotropic effect for Hemin. According to surgery and treatment procedures, mices were divided into five groups: Control, Ischemia-reperfusion injury (IRI), animals pre-treated with Hemin followed by IRI (Hemin + IRI), animals only treated with Hemin (Hemin) and animals pre-conditioned and submitted to IRI (IPC+IRI). To identify the consequences of IRI, Hemin treatment or IPC in gene expression profiles, the following statistical comparisons were made between the groups: IRI vs Control, IPC+IRI vs Control, IPC+IRI vs IRI, IRI+Hemin vs IRI and Hemin vs Control.
2012-12-10 | E-GEOD-39548 | biostudies-arrayexpress
Project description:The clear benefits of ischemic preconditioning (IPC) in reducing ischemia reperfusion injury (IRI) remain indistinct in human liver transplantation. To further understand the mechanistic aspects of IPC in human deceased donor liver transplantation (DDLT), we performed microarray analyses to determine global gene expression profiles associated with IPC administration. Donor and recipient characteristics in both groups were comparable. Clinical data from our study subset and larger trial were similar. IPC increased expression of 10 transcripts at either time point with roles in: antioxidant defenses, immunological response, lipid biosynthesis, and xenobiotic metabolism. IPC decreased the expression of 1 cell development related transcript. Conclusions: 1) IPC in DDLT increased the expression of antioxidant transcripts similar to studies in animal IPC, anesthetic, and remote IPC. 2) IPC increased expression of lipogenic transcripts, which may be relevant to the clinically observed increased IRI in our IPC group. 3) Our microarray findings support our clinical observations and are compatible with the varied outcomes of hepatic IPC studies in human liver transplantation.
2009-04-01 | GSE15480 | GEO
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
Project description:The clear benefits of ischemic preconditioning (IPC) in reducing ischemia reperfusion injury (IRI) remain indistinct in human liver transplantation. To further understand the mechanistic aspects of IPC in human deceased donor liver transplantation (DDLT), we performed microarray analyses to determine global gene expression profiles associated with IPC administration. Donor and recipient characteristics in both groups were comparable. Clinical data from our study subset and larger trial were similar. IPC increased expression of 10 transcripts at either time point with roles in: antioxidant defenses, immunological response, lipid biosynthesis, and xenobiotic metabolism. IPC decreased the expression of 1 cell development related transcript. Conclusions: 1) IPC in DDLT increased the expression of antioxidant transcripts similar to studies in animal IPC, anesthetic, and remote IPC. 2) IPC increased expression of lipogenic transcripts, which may be relevant to the clinically observed increased IRI in our IPC group. 3) Our microarray findings support our clinical observations and are compatible with the varied outcomes of hepatic IPC studies in human liver transplantation. We conducted a nested sub-study in 12/101 subjects enrolled in a prospective randomized trial of 10 min IPC in DDLT during 2003-2006. Liver biopsies were performed at the end of cold storage and at 90 minutes after allograft reperfusion. Six biopsy pairs from both IPC and No IPC (STD) groups within a narrow donor risk index range were selected. Total RNA was extracted and hybridized with Affymetrix GeneChip Human Gene 1.0 ST Array. IPC effects were examined by comparing IPC vs. STD at both time points. Transcripts whose expression changed 2-fold with p<0.05 were considered significant.
2010-05-20 | E-GEOD-15480 | biostudies-arrayexpress
Project description:To investigate the mechanism by which ischemic preconditioning (IPC) produces tissue tolerance to renal ischemia reperfusion injury in a pig model 15 female Yorkshire pigs were divided into three groups: 1: no IPC and 90 minutes warm ischemia; 2: remote IPC with an early window followed by 90 min warm ischemia; 3: remote IPC with a late window followed by warm ischemia 24 hrs later. Kidney tissues were obtained after 72 hours.
2016-09-02 | E-GEOD-72646 | biostudies-arrayexpress
Project description:To investigate the mechanism by which ischemic preconditioning (IPC) produces tissue tolerance to renal ischemia reperfusion injury in a pig model
2016-09-02 | GSE72646 | GEO
Project description:We examined, through an oligonucleotide microarray protocol, the renal differential transcriptome profiles of mices submitted to IRI, IPC and Hemin treatment. After identifying the profiles of differentially expressed genes observed for each comparison, we carried out functional enrichment analysis to reveal transcripts putatively involved in potential relevant biological processes and signaling pathways. The most relevant enriched biological processes found in these comparisons were stress, inflammation, apoptosis, pathways in cancer, differentiation, angiogenesis, focal adhesion, ECM-receptor interaction, ion transport, angiogenesis, mitosis and cell cycle, inflammatory response, olfactory transduction and regulation of actin cytoskeleton. In addition, the most important overrepresented pathways were MAPK, ErbB, JAK/STAT, Toll and Nod like receptors, Angiotensin II, Arachidonic acid metabolism, Wnt and coagulation cascade. Also, new insights were gained about the underlying protection mechanisms against renal IRI promoted by IPC and Hemin treatment. Venn diagram analysis allowed us to uncover common and exclusively differentially expressed genes between these two protective maneuvers, underscoring potential common and exclusive biological functions regulated in each case. In summary, IPC exclusively regulated the expression of genes belonging to stress, protein modification and apoptosis, highlighting the role of IPC in controlling exacerbated stress response. Treatment with the Hmox1 inducer Hemin, in turn, exclusively regulated the expression of genes associated with cell differentiation, metabolic pathways, cell cycle, mitosis, development, regulation of actin cytoskeleton and arachidonic acid metabolism, suggesting a pleiotropic effect for Hemin.
2012-12-10 | GSE39548 | GEO
Project description:Circular RNA microarray analyses in hepatic ischemia-reperfusion injury with ischemic preconditioning prevention
| PRJNA690117 | ENA
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.
2011-10-01 | GSE24430 | GEO
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