A Molecular signature for Delayed Graft Function
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA356242 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5076690.fastq.gz | Fastqsanger.gz | |||
| SRR5076690_1.fastq.gz | Fastqsanger.gz | |||
| SRR5076690_2.fastq.gz | Fastqsanger.gz | |||
| SRR5076700.fastq.gz | Fastqsanger.gz | |||
| SRR5076700_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The aim of this study was to identify a molecular signature for extreme DGF in a retrospective analysis of paired renal allograft biopsies obtained at two time points: pre-implantation during preparatory phase (pre-perfusion biopsies, b) and after reperfusion when circulation was restored (post-perfusion biopsies , b1).
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Project description:Purpose: The aim of this study was to identify a molecular signature for extreme DGF in a retrospective analysis of paired renal allograft biopsies obtained at two time points: pre-implantation during preparatory phase (pre-perfusion biopsies, b) and after reperfusion when circulation was restored (post-perfusion biopsies , b1).
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Project description:Purpose: The aim of this study was to identify a molecular signature for extreme DGF in a retrospective analysis of paired renal allograft biopsies obtained at two time points: pre-implantation during preparatory phase (pre-perfusion biopsies, b) and after reperfusion when circulation was restored (post-perfusion biopsies , b1).
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Project description:Delayed graft function (DGF) is associated with a reduced graft survival. Donors' features have been always considered as key pathogenic factors in this setting. The aim of our study was to evaluate the role of recipients' characteristics in the development of DGF. We prospectively enrolled 932 kidney graft recipients from 466 donors. A total of 226 recipients experienced DGF. Among the 466 donors, in 290 both recipients presented with early graft function (EGF, group A), in 50 both recipients experienced DGF (group B) and in 126 one recipient presented with DGF and the other with EGF (group C). In group C we randomly selected 7 couples of DGF/EGF recipients. In these patients, circulating mononuclear cells were harvested before transplantation and their transcriptomic profile was investigated by a microarray approach. Results were validated by qPCR in an independent group of EGF/DGF couples.
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Project description:Chronic kidney disease and associated comorbidities (diabetes, cardiovascular diseases) manifest with an accelerated ageing phenotype, leading ultimately to organ failure and renal replacement therapy. This process can be modulated by epigenetic and environmental factors which promote loss of physiological function and resilience to stress earlier, linking biological age with adverse outcomes post-transplantation including delayed graft function (DGF). The molecular features underpinning this have yet to be fully elucidated. We have determined a molecular signature for loss of resilience and impaired physiological function, via a synchronous genome, transcriptome and proteome snapshot, using human renal allografts as a source of healthy tissue as an in vivo model of ageing in humans. This comprises 42 specific transcripts, related through IFN? signalling, which in allografts displaying clinically impaired physiological function (DGF) exhibited a greater magnitude of change in transcriptional amplitude and elevated expression of noncoding RNAs and pseudogenes, consistent with increased allostatic load. This was accompanied by increased DNA methylation within the promoter and intragenic regions of the DGF panel in preperfusion allografts with immediate graft function. Pathway analysis indicated that an inability to sufficiently resolve inflammatory responses was enabled by decreased resilience to stress and resulted in impaired physiological function in biologically older allografts. Cross-comparison with publically available data sets for renal pathologies identified significant transcriptional commonality for over 20 DGF transcripts. Our data are clinically relevant and important, as they provide a clear molecular signature for the burden of "wear and tear" within the kidney and thus age-related physiological capability and resilience.
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Project description:A Molecular signature for Delayed Graft Function [BS-Seq]
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Project description:A Molecular signature for Delayed Graft Function (miRNA-Seq)
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Project description:A Molecular signature for Delayed Graft Function [RNA-Seq]
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Project description:Delayed graft function (DGF) is associated with a reduced long-term graft survival. Ischemia-reperfusion damage and donors' features have been always considered as key pathogenic factors in this setting. The aim of our study was to evaluate the role of recipients' characteristics in the development of DGF to discover early genomics biomarkers in peripheral blood mononuclear cells (PBMC) in order to identify patients at risk. We prospectively enrolled 932 kidney graft recipients from 466 donors for both kidneys. A total of 226 recipients experienced DGF. Among the 466 donors, 290 couples of recipients both patients presented with early graft function (EGF, group A), 50 couples experienced DGF (group B) and 126 couples of recipients were discordant as one presented DGF and the other promptly recovered graft function (group C). In group C we randomly selected 10 couples of DGF/EGF recipients. Peripheral blood mononuclear cells (PBMC) were harvested before transplantation; their transcriptomic profile was investigated by a microarray approach and microarray results were validated by qPCR in an independent group (DGF n=25; EGF n=25). In the whole study group, DGF was independently associated with both donors’ and recipient’s features. Moreover, group A, B and C presented significant differences in both donors’ and recipients’ characteristics. In group C of patients, DGF was significantly associated with body mass index, dialysis modality and number of mismatches. Two-hundred and seventy-three genes were differentially expressed before transplantation in discordant EGF/DGF patients of group C. Their main biological functions were immune dysfunction and inflammation. Among the differentially expressed genes, we observed a significant increase in the expression of CCR2, the MCP-1 receptor, in DGF patients. CCR-2 and MCP-1 up-regulation was confirmed in an independent cohort of patients. Our results suggest that recipients' clinical and immunological features, potentially modulated by dialysis modality, are associated with the development of DGF independently of donors' features.
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