Kinetic of gene expression signatures on ischemia porcine kidney
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PROVIDER: PRJNA431790 | ENA |
REPOSITORIES: ENA
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Project description:Using an oligonucleotide microarray we performed differential transcriptomic analysis of porcine kidneys subjected to intense ischemic stress which could be observed in donors deceased after circulatory death situation (60 min warm ischemia then 24h of cold storage in University of Wisconsin solution) compared to healthy kidneys (n=3). 43 genes were differentially expressed in ischemic versus healthy kidneys (adjusted p value <0.05 + log2 fold change >0.5 or <-0.5). Functional enrichment analysis via Gene ontology revealed relevant biological processes and signaling pathways such as: cellular responses to stress and cell cycle adaptation, metabolism modification, RNA reprograming, cellular phenotype changes and inflammation. Our data showed that ischemia is a dynamic process, with important transcriptional modifications on major pathways. We uncovered a number of targets which we will further validate as biomarkers and therapeutic targets to optimize organ quality. ISCHEMIA samples: Three independent porcine kidney (from different Large White pig) were clamped, removed and maintained clamped 60 min at 37°C, and then flushed with cold (4°C) University of Wisconsin preservation solution (UW) and stored at 4°C for 24h, then kidneys were immediatly sampled and frozen. CONTROL samples: Three independent porcine kidney (from different Large White pig) were removed and then immediatly sampled and frozen.
2016-03-22 | E-GEOD-79418 | biostudies-arrayexpress
Project description:Using an oligonucleotide microarray we performed differential transcriptomic analysis of porcine kidneys subjected to intense ischemic stress which could be observed in donors deceased after circulatory death situation (60 min warm ischemia then 0h, 6h or 24h of cold storage in University of Wisconsin solution) compared to healthy kidneys (n=5 per group). Microarray analysis identified genes which were differentially expressed in different ischemic times versus healthy kidneys (adjusted p value <0.05 + log2 fold change >0.5 or <-0.5).
2018-02-10 | GSE109719 | GEO
Project description:Using an oligonucleotide microarray we performed differential transcriptomic analysis of porcine kidneys subjected to intense ischemic stress which could be observed in donors deceased after circulatory death situation (60 min warm ischemia then 24h of cold storage in University of Wisconsin solution) compared to healthy kidneys (n=3). 43 genes were differentially expressed in ischemic versus healthy kidneys (adjusted p value <0.05 + log2 fold change >0.5 or <-0.5). Functional enrichment analysis via Gene ontology revealed relevant biological processes and signaling pathways such as: cellular responses to stress and cell cycle adaptation, metabolism modification, RNA reprograming, cellular phenotype changes and inflammation. Our data showed that ischemia is a dynamic process, with important transcriptional modifications on major pathways. We uncovered a number of targets which we will further validate as biomarkers and therapeutic targets to optimize organ quality.
2016-03-22 | GSE79418 | GEO
Project description:Background: Remote Ischemic Conditioning (RIC) has been proposed as a therapeutic intervention to circumvent the Ischemia/reperfusion injury (IRI) that is inherent to organ transplantation. Using a porcine kidney transplant model, we aimed to decipher the subclinical molecular effects of a RIC regime, compared to non-RIC controls. Methods: Kidney pairs (n = 8+8) were extracted from brain dead donor pigs and transplanted in juvenile recipient pigs following a period of cold ischemia. One of the two kidney recipients in each pair was subjected to RIC prior to kidney graft reperfusion, while the other served as non-RIC control. We designed a modern integrative Omics strategy combining transcriptomics, proteomics, and phosphoproteomics to deduce molecular signatures in kidney tissue that could be attributed to RIC. Results: In kidney grafts taken out 10 h after transplantation we detected minimal molecular perturbations following RIC compared to non-RIC at the transcriptome level, which was mirrored at the proteome level. In particular, we noted that RIC resulted in suppression of tissue inflammatory profiles. Furthermore, an accumulation of muscle extracellular matrix assembly proteins in kidney tissues was detected at the protein level, which may be in response to muscle tissue damage and/or fibrosis. Conclusions: Our data identifies subtle molecular phenotypes in porcine kidneys following RIC and this knowledge could potentially aid optimisation of remote ischaemia protocols in renal transplantation.
2021-09-04 | E-MTAB-10872 | biostudies-arrayexpress
Project description:Background: Remote Ischemic Conditioning (RIC) has been proposed as a therapeutic intervention to circumvent the Ischemia/reperfusion injury (IRI) that is inherent to organ transplantation. Using a porcine kidney transplant model, we aimed to decipher the subclinical molecular effects of a RIC regime, compared to non-RIC controls. Methods: Kidney pairs (n = 8+8) were extracted from brain dead donor pigs and transplanted in juvenile recipient pigs following a period of cold ischemia. One kidney in each pair was subjected to RIC prior to reperfusion, while the other served as non-RIC control. We designed an advanced integrative -Omics strategy combining transcriptomics, proteomics, and phosphoproteomics to deduce molecular signatures in kidney tissue that could be attributed to RIC. Results: In kidney grafts taken out 10 h after transplantation we detected minimal molecular perturbations following RIC compared to non-RIC at the transcriptome level, but more pronounced effects at the proteome level. In particular, we noted that RIC resulted in response suppression of tissue inflammatory profiles. Furthermore, an accumulation of muscle extracellular matrix assembly proteins in RIC tissues was detected at the protein level, which may result in response to muscle tissue damage and/or fibrosis. Conclusions: Our data identifies subtle molecular phenotypes in porcine kidneys subjected to RIC which could aid further optimisation of remote ischaemia protocols in renal transplantation.
2022-04-04 | PXD025273 | Pride
Project description:Purpose: Acute kidney injury (AKI) is defined as a sudden event of kidney failure or kidney damage occurring within a short period. Ischemia-reperfusion injury (IRI) is a critical factor to induce severe AKI and end-stage kidney disease in the kidney. However, biological mechanisms of ischemia and reperfusion are not well elucidated due to its complex pathophysiological processes. We aim to investigate key biological pathways affected by ischemia and by reperfusion separately at the transcriptome level. Method: We analyzed steady-state gene expressions using RNA-seq transcriptome data for normal (pre-ischemia), ischemia and reperfusion conditions obtained from the human kidney tissue. A conventional differential expression analysis and self-organizing map (SOM) clustering analysis followed by pathway analysis were performed to identify the underlying biological mechanisms of ischemia and reperfusion. Results: Differential expression analysis showed that metabolism and gap junction-related pathways were dysregulated in ischemia, whereas hypertrophy and immune response-related pathways were dysregulated in reperfusion. In addition, SOM clustering analysis revealed that metabolism, apoptosis, and fibrosis-related pathways were significantly dysregulated by ischemia compared to pre-ischemia. On the other hand, cell growth, migration, and immune response-related pathways were highly dysregulated by reperfusion after ischemia. Pro-apoptotic genes and death receptors were down-regulated during ischemia, indicating a protective process against ischemic injury. Reperfusion induced alteration of genes associated with immune components such as B-cell, neutrophil, and interleukin-15. Additionally, genes related to cell growth and migration such as AKT, KRAS, and Rho signaling were down-regulated, which might imply injury responses during reperfusion. Semaphorin 4D and plexin B1 were also down-regulated. However, further investigations are needed to identify their roles. Conclusion: We showed that specific biological pathways were distinctively involved in ischemia and reperfusion during IRI, suggesting that condition-specific therapeutic strategies may be required to prevent severe kidney damage after IRI in clinical research.
2019-12-17 | GSE142077 | GEO
Project description:Mouse kidney ischemia-reperfusion injury time course
| PRJNA1112333 | ENA
Project description:RNA-Seq identifies condition-specific biological signatures of ischemia-reperfusion injury in the human kidney
| PRJNA595865 | ENA
Project description:Gene expression signatures of ischemia on porcine kidney
| PRJNA315811 | ENA
Project description:Purpose: we performed comparative RNA-seq analyses to identify molecular network characteristics of kidney injury at different ischemia times Methods: Unilateral clamping of the left renal pedicle plus contralateral nephrectomy was performed. Briefly, mice were anesthetized, right kidney was excised. The left kidney was clamped for indicated minutes (0min for sham-24h group, 16min for uIRIx16min-24h group, 18minfor uIRIx18min-24h group, 20min for uIRIx20min-24h group, 22min for uIRIx22min-24h group, 24min for uIRIx24min-24h group, 26min for uIRIx26min-24h group, 28min for uIRIx28min-24h group, 30min for uIRIx30min-24h group). Mice were placed on 37°C heating platform while operation, ischemia and before awakening. At 24h after ischemia, mice were anesthetized and blood was taken to detect creatinine, kidney was harvest for PAS staining and mRNA seq. Results: After sequence, the clean reads rate of all samples were ≥98%.The quality of the assembled transcriptome is good enough for functional annotation and further analysis. Conclusions: We performed RNA-sequencing (RNA-Seq) analyses to identify molecular network characteristics of kidney injury at different ischemia time.
2022-01-04 | GSE192883 | GEO