Recapitulation of premature ageing with iPSCs from Hutchinson-Gilford progeria syndrome
Open accessAbstract
Hutchinson-Gilford progeria syndrome (HGPS) is a rare and fatal human premature ageing disease, characterized by premature arteriosclerosis and degeneration of vascular smooth muscle cells (SMCs). HGPS is caused by a single point mutation in the lamin A (LMNA) gene, resulting in the generation of progerin, a truncated splicing mutant of lamin A. Accumulation of progerin leads to various ageing-associated nuclear defects including disorganization of nuclear lamina and loss of heterochromatin. Here we report the generation of induced pluripotent stem cells (iPSCs) from fibroblasts obtained from patients with HGPS. HGPS-iPSCs show absence of progerin, and more importantly, lack the nuclear envelope and epigenetic alterations normally associated with premature ageing. Upon differentiation of HGPS-iPSCs, progerin and its ageing-associated phenotypic consequences are restored. Specifically, directed differentiation of HGPS-iPSCs to SMCs leads to the appearance of premature senescence phenotypes associated with vascular ageing. Additionally, our studies identify DNA-dependent protein kinase catalytic subunit (DNAPKcs, also known as PRKDC) as a downstream target of progerin. The absence of nuclear DNAPK holoenzyme correlates with premature as well as physiological ageing. Because progerin also accumulates during physiological ageing, our results provide an in vitro iPSC-based model to study the pathogenesis of human premature and physiological vascular ageing.
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HGPS fibroblasts present biomarkers of aging and senescence.
“To determine if sEV-Ys within the CM had the potential to ameliorate biomarkers of aging, we took advantage of primary fibroblasts derived from patients with a severe form of premature aging, HGPS, which present biomarkers of aging and senescence (Figure S2A) (Burtner and Kennedy, 2010, Ocampo et al., 2016, Liu et al., 2011).”
From Small Extracellular Vesicles Have GST Activity and Ameliorate Senescence-Related Tissue Damage (2020) · cites this paper as Liu et al., 2011
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- Authors
- Liu, G.-H., Barkho, B. Z., Ruiz, S., Diep, D., Qu, J., Yang, S.-L., Panopoulos, A. D., Suzuki, K., Kurian, L., Walsh, C., Thompson, J., Boue, S., Fung, H. L., Sancho-Martinez, I., Zhang, K., Yates, J. Y., & Belmonte, J. C. I.
- Affiliations
- Salk Institute for Biological Studies (US)
- University of California San Diego (US)
- Scripps Research Institute (US)
- ORCID
- Venue
- Nature
- Published
- 2011-02-23
- Volume
- 472
- Issue
- 7342
- Pages
- 221-225
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3088088
- OpenAlex
- W2073610802
- Cited by
- 575
- References
- 42
- Citations by year
- 2026: 21 · 2025: 20 · 2024: 16 · 2023: 24 · 2022: 33 · 2021: 32 · 2020: 48 · 2019: 31 · 2018: 43 · 2017: 40 · 2016: 38 · 2015: 42 · 2014: 42 · 2013: 39 · 2012: 62
- FWCI
- 24.30
- Type
- journal article
- Language
- en
- Update notices
- correction (2025-04-07)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- National Institute on Drug Abuse (R01DA025779)
- National Cancer Institute (T32CA009370)
- National Center for Research Resources (P41RR011823)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- Hutchinson-Gilford progeria syndrome, premature aging, induced pluripotent stem cells, lamin A, progerin, vascular smooth muscle cells, premature senescence, vascular aging, PRKDC, nuclear lamina, epigenetic modifications, fibroblast reprogramming
- MeSH terms
- Calponins, Aging, Calcium-Binding Proteins, Cell Differentiation, Cell Line, Fibroblasts, Humans, Microfilament Proteins, Models, Biological, Muscle, Smooth, Vascular, Nuclear Envelope, Nuclear Proteins, Phenotype, Progeria, Protein Precursors, Substrate Specificity, Cellular Senescence, Aging, Premature, Holoenzymes, Lamin Type A, Epigenesis, Genetic, DNA-Activated Protein Kinase, Induced Pluripotent Stem Cells, Cellular Reprogramming
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