Proteomic Evidence of Biological Aging in a Child with a Compound Heterozygous ZMPSTE24 Mutation.


Journal

Proteomics. Clinical applications
ISSN: 1862-8354
Titre abrégé: Proteomics Clin Appl
Pays: Germany
ID NLM: 101298608

Informations de publication

Date de publication:
03 2019
Historique:
received: 16 08 2018
revised: 03 12 2018
pubmed: 15 12 2018
medline: 3 5 2019
entrez: 15 12 2018
Statut: ppublish

Résumé

Progeria-like syndromes offer a unique insight into aging. Here the case of a boy affected with mandibuloacral dysplasia and compound heterozygous mutations in ZMPSTE24 is presented. Capillary electrophoresis-mass spectroscopy is used for proteome analysis to analyze peptides previously found to be differentially regulated in chronic kidney disease (273 peptides defining the CKD273 classifier), coronary artery disease (238 peptides defining the CAD238 classifier), and aging (116 peptides defining the AGE116 classifier). No evidence of renal disease is identified. Although the boy has no overt cardiovascular disease other than a raised carotid intima media thickness relative to his age, a proteomic classifier for the diagnosis of coronary artery disease is mildly raised. The biological age based on the proteomic AGE116 classifier is 24 years compared to the chronological ages of 5 and 10 years. In contrast, a control group of healthy children has a significantly lower (p < 0.0001) calculated mean age of 13. Urinary proteomic analysis is effective in confirming advanced biological age and to identify early evidence of renal or cardiovascular damage. This case highlights the value of proteomic approaches in aging research and may represent a method for non-invasive monitoring of the effects of early aging.

Sections du résumé

BACKGROUND
Progeria-like syndromes offer a unique insight into aging. Here the case of a boy affected with mandibuloacral dysplasia and compound heterozygous mutations in ZMPSTE24 is presented.
METHODS
Capillary electrophoresis-mass spectroscopy is used for proteome analysis to analyze peptides previously found to be differentially regulated in chronic kidney disease (273 peptides defining the CKD273 classifier), coronary artery disease (238 peptides defining the CAD238 classifier), and aging (116 peptides defining the AGE116 classifier).
RESULTS
No evidence of renal disease is identified. Although the boy has no overt cardiovascular disease other than a raised carotid intima media thickness relative to his age, a proteomic classifier for the diagnosis of coronary artery disease is mildly raised. The biological age based on the proteomic AGE116 classifier is 24 years compared to the chronological ages of 5 and 10 years. In contrast, a control group of healthy children has a significantly lower (p < 0.0001) calculated mean age of 13.
CONCLUSION
Urinary proteomic analysis is effective in confirming advanced biological age and to identify early evidence of renal or cardiovascular damage. This case highlights the value of proteomic approaches in aging research and may represent a method for non-invasive monitoring of the effects of early aging.

Identifiants

pubmed: 30548811
doi: 10.1002/prca.201800135
pmc: PMC6492098
doi:

Substances chimiques

Membrane Proteins 0
Metalloendopeptidases EC 3.4.24.-
ZMPSTE24 protein, human EC 3.4.24.84

Types de publication

Case Reports Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1800135

Subventions

Organisme : Medical Research Council
ID : MR/N003403/1
Pays : United Kingdom
Organisme : European Commission
ID : 603288
Pays : International
Organisme : British Heart Foundation
ID : RE/13/5/30177
Pays : United Kingdom

Informations de copyright

© 2018 The Authors. Proteomics - Clinical Application published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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Auteurs

Angela K Lucas-Herald (AK)

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, G12 8TA, UK.
Developmental Endocrinology Research Group, School of Medicine, University of Glasgow, Glasgow, G51 4TF, UK.

Petra Zürbig (P)

Mosaiques Diagnostics GmbH, Rotenburger Str. 20, 30659, Hannover, Germany.

Avril Mason (A)

Developmental Endocrinology Research Group, School of Medicine, University of Glasgow, Glasgow, G51 4TF, UK.

Esther Kinning (E)

Department of Clinical Genetics, Queen Elizabeth University Hospital, Glasgow, G51 4TF, UK.

Catriona E Brown (CE)

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, G12 8TA, UK.

Bahareh Mansoorian (B)

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, G12 8TA, UK.

William Mullen (W)

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, G12 8TA, UK.

Syed Faisal Ahmed (SF)

Developmental Endocrinology Research Group, School of Medicine, University of Glasgow, Glasgow, G51 4TF, UK.

Christian Delles (C)

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, G12 8TA, UK.

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