Cited by 781Pluripotent Stem Cells ResearchParkinson's Disease Mechanisms and TreatmentsGenetics, Aging, and Longevity in Model Organisms

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Human iPSC-Based Modeling of Late-Onset Disease via Progerin-Induced Aging

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Miller, Justine D., Ganat, Yosif M., Kishinevsky, Sarah, Bowman, Robert L., Liu, Becky, Tu, Edmund Y., Mandal, Pankaj K., Vera, Elsa, Shim, Jae-won, Kriks, Sonja, Taldone, Tony, Fusaki, Noemi, Tomishima, Mark J., Krainc, Dimitri, Milner, Teresa A., Rossi, Derrick J., Studer, Lorenz·2013·Cell stem cell

DOI 10.1016/j.stem.2013.11.006PMC PMC4153390

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Abstract

Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders. In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD). Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging. We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation. Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions. Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.

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Authors: Miller, J. D., Ganat, Y. M., Kishinevsky, S., Bowman, R. L., Liu, B., Tu, E. Y., Mandal, P. K., Vera, E., Shim, J.-W., Kriks, S., Taldone, T., Fusaki, N., Tomishima, M. J., Krainc, D., Milner, T. A., Rossi, D. J., & Studer, L.
Affiliations: Memorial Sloan Kettering Cancer Center (US)
Boston Children's Hospital (US)
Keio University (JP)
Harvard University (US)
Weill Cornell Medicine (US)
Corresponding author: Studer, Lorenz
ORCID: Bowman, Robert L.
Liu, Becky
Mandal, Pankaj K.
Krainc, Dimitri
Milner, Teresa A.
Rossi, Derrick J.
Studer, Lorenz
Venue: Cell stem cell
Publisher: Elsevier BV
Published: 2013-12
Volume: 13
Issue: 6
Pages: 691-705
ISSN: 1875-9777 (ISSN-L)
1934-5909
DOI: 10.1016/j.stem.2013.11.006
PMC: PMC4153390
OpenAlex: W2081914422
Cited by: 777
References: 291
Citations by year: 2026: 46 · 2025: 41 · 2024: 52 · 2023: 54 · 2022: 50 · 2021: 71 · 2020: 66 · 2019: 64 · 2018: 76 · 2017: 72 · 2016: 94 · 2015: 52 · 2014: 38 · 2013: 1
FWCI: 27.60
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 369 d)
Locations: Cell stem cell (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Science Foundation
New York Stem Cell Foundation
Memorial Sloan-Kettering Cancer Center
National Institutes of Health
National Heart, Lung, and Blood Institute (HL-098351, R01HL098351)
National Institute on Drug Abuse (R01DA008259, DA08259)
National Cancer Institute (F31CA167863, P30CA008748)
National Institute of Neurological Disorders and Stroke (NS078338, U24NS078338, R01NS052671, R01NS076054, NS076054)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords: progerin, lamin A, premature aging, induced pluripotent stem cells, Parkinson's disease, late-onset disease, iPSC-derived fibroblasts, dendrite degeneration, tyrosine hydroxylase, Lewy bodies, mitochondrial enlargement, disease modeling
MeSH terms: Adult, Aged, Aged, 80 and over, Aging, Animals, Cell Differentiation, Child, Fibroblasts, Humans, Mesencephalon, Middle Aged, Models, Biological, Nuclear Proteins, Parkinson Disease, Phenotype, Protein Precursors, Tissue Donors, Biomarkers, Cellular Senescence, Age of Onset, Lamin Type A, Mice, Induced Pluripotent Stem Cells, Dopaminergic Neurons, Cellular Reprogramming

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Human iPSC-Based Modeling of Late-Onset Disease via Progerin-Induced Aging

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