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).
2019-01-18 | GSE90863 | GEO
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:This SuperSeries is composed of the SubSeries listed below.
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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 IFNγ 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:The frequency of delayed function of kidney transplants varies greatly and is associated with the quality of graft, donor age, and the duration of cold ischemia time. Body weight differences between donor and recipient can affect primary graft function. The underlying mechanism is poorly understood. Here, we have transplanted kidney grafts from commensurate body weight (L-WD) or reduced body weight (H-WD) donor rats into syngeneic or allogeneic recipients. 24 hours post-transplantation, serum creatinine level in H-WD recipients was significantly higher compared to that of L-WD recipients indicating impaired primary graft function. We detected a 10 fold higher transcription of IL-6 and dramatically increased tubular destruction in grafts from H-WD recipients. This was accompanied by decreased expression of genes associated with kidney function and an up-regulation of other genes such as cytochrome P450 isoforms, FosL and Trib3 as revealed by DNA microarray analysis. A single application of IL-6 into L-WD recipients is sufficient to impair primary graft function and to cause tubular damage. Whereas, immediate neutralization of IL-6 receptor signaling rescued primary graft function resulting in low serum creatinine levels, well-preserved kidney graft architecture and a normalized gene expression profile. These findings have strong clinical implication as anti-IL6R treatment of patients receiving grafts from lower-weight donors could be used to improve primary graft function. The dataset comprises eight samples divided into four sample groups. Each group represents rat kidneys collected after allogeneic transplantation under a certain condition and includes two biological replicates. The first group is characterized by a high body weight difference between donor and recipient, rats in the second group exhibit a low weight difference. Group three and four are similar to group one, but underwent an additional treatment with anti-IL6R mAb or prednisolone immediately after transplantation.
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