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A multi-omics longitudinal aging dataset in primary human fibroblasts with mitochondrial perturbations.

Published version
Peer-reviewed

Type

Article

Change log

Authors

Monzel, Anna S 
Karan, Kalpita R 
Michelson, Jeremy 
Ware, Sarah A 

Abstract

Aging is a process of progressive change. To develop biological models of aging, longitudinal datasets with high temporal resolution are needed. Here we report a multi-omics longitudinal dataset for cultured primary human fibroblasts measured across their replicative lifespans. Fibroblasts were sourced from both healthy donors (n = 6) and individuals with lifespan-shortening mitochondrial disease (n = 3). The dataset includes cytological, bioenergetic, DNA methylation, gene expression, secreted proteins, mitochondrial DNA copy number and mutations, cell-free DNA, telomere length, and whole-genome sequencing data. This dataset enables the bridging of mechanistic processes of aging as outlined by the "hallmarks of aging", with the descriptive characterization of aging such as epigenetic age clocks. Here we focus on bridging the gap for the hallmark mitochondrial metabolism. Our dataset includes measurement of healthy cells, and cells subjected to over a dozen experimental manipulations targeting oxidative phosphorylation (OxPhos), glycolysis, and glucocorticoid signaling, among others. These experiments provide opportunities to test how cellular energetics affect the biology of cellular aging. All data are publicly available at our webtool: https://columbia-picard.shinyapps.io/shinyapp-Lifespan_Study/.

Description

Keywords

Humans, Aging, Fibroblasts, Longevity, Cellular Senescence, Glycolysis

Journal Title

Sci Data

Conference Name

Journal ISSN

2052-4463
2052-4463

Volume Title

9

Publisher

Springer Science and Business Media LLC
Sponsorship
U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) (AG066828)
U.S. Department of Health &amp (AG066828)