A molecular signature for delayed graft function

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 physio...

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Published inAging cell Vol. 17; no. 5; pp. e12825 - n/a
Main Authors McGuinness, Dagmara, Mohammed, Suhaib, Monaghan, Laura, Wilson, Paul A., Kingsmore, David B., Shapter, Oliver, Stevenson, Karen S., Coley, Shana M., Devey, Luke, Kirkpatrick, Robert B., Shiels, Paul G.
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.10.2018
John Wiley and Sons Inc
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Abstract 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.
AbstractList 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.
Audience Academic
Author Monaghan, Laura
Wilson, Paul A.
Kingsmore, David B.
Shapter, Oliver
McGuinness, Dagmara
Devey, Luke
Mohammed, Suhaib
Stevenson, Karen S.
Kirkpatrick, Robert B.
Shiels, Paul G.
Coley, Shana M.
AuthorAffiliation 1 Wolfson Wohl Translational Research Centre, Institute of Cancer Sciences, College of Medical, Veterinary & Life Sciences University of Glasgow Glasgow UK
4 Research Institute of Infection Immunity and Inflammation, College of Medical, Veterinary & Life Sciences University of Glasgow Glasgow UK
6 The Pipeline Futures Group GlaxoSmithKline Collegeville Pennsylvania
9 Present address: Paul O'Gorman Leukaemia Research Centre Gartnavel General Hospital Glasgow UK
3 Renal Transplant Unit, NHS Greater Glasgow and Clyde South Glasgow University Hospital Glasgow UK
5 Metabolic Pathways Cardio Therapy Area Unit GlaxoSmithKline King of Prussia Pennsylvania
7 Present address: Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary & Life Sciences University of Glasgow Glasgow UK
8 Present address: The European Bioinformatics Institute (EMBL‐EBI) Saffron Walden UK
2 Computational Biology GlaxoSmithKline Medicines Research Centre Steven
AuthorAffiliation_xml – name: 7 Present address: Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary & Life Sciences University of Glasgow Glasgow UK
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ContentType Journal Article
Copyright 2018 The Authors. published by the Anatomical Society and John Wiley & Sons Ltd.
2018 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
COPYRIGHT 2018 John Wiley & Sons, Inc.
Copyright © 2018 The Anatomical Society and John Wiley & Sons Ltd.
Copyright_xml – notice: 2018 The Authors. published by the Anatomical Society and John Wiley & Sons Ltd.
– notice: 2018 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
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– notice: Copyright © 2018 The Anatomical Society and John Wiley & Sons Ltd.
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Snippet Chronic kidney disease and associated comorbidities (diabetes, cardiovascular diseases) manifest with an accelerated ageing phenotype, leading ultimately to...
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StartPage e12825
SubjectTerms Adult
Aged
Aging
Allografts
Alternative Splicing - genetics
Analysis
Cardiovascular diseases
Cellular Senescence - genetics
Chronic kidney failure
Cohort Studies
Delayed Graft Function - genetics
Delayed Graft Function - immunology
Delayed Graft Function - pathology
Diabetes mellitus
DNA methylation
Environmental factors
Epigenesis, Genetic
Epigenetics
Female
Gene expression
Gene Expression Profiling
Genomes
Humans
Inflammation
Kidney transplantation
Kidneys
Male
Middle Aged
Original
Perfusion
Phenotypes
Physiological aspects
Physiology
Proteomes
Pseudogenes
Renal failure
Reperfusion Injury - genetics
Reproducibility of Results
RNA, Messenger - genetics
RNA, Messenger - metabolism
Sequence Analysis, RNA
Signal transduction
Transcription
Transplantation
Type 2 diabetes
γ-Interferon
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Title A molecular signature for delayed graft function
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Facel.12825
https://www.ncbi.nlm.nih.gov/pubmed/30094915
https://www.proquest.com/docview/2112029348
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https://pubmed.ncbi.nlm.nih.gov/PMC6156499
Volume 17
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