Oxidative stress-associated senescence in dermal papilla cells of men with androgenetic alopecia
Open accessAbstract
Dermal papilla cells (DPCs) taken from male androgenetic alopecia (AGA) patients undergo premature senescence in vitro in association with the expression of p16(INK4a), suggesting that DPCs from balding scalp are more sensitive to environmental stress than nonbalding cells. As one of the major triggers of senescence in vitro stems from the cell "culture shock" owing to oxidative stress, we have further investigated the effects of oxidative stress on balding and occipital scalp DPCs. Patient-matched DPCs from balding and occipital scalp were cultured at atmospheric (21%) or physiologically normal (2%) O2. At 21% O2, DPCs showed flattened morphology and a significant reduction in mobility, population doubling, increased levels of reactive oxygen species and senescence-associated β-Gal activity, and increased expression of p16(INK4a) and pRB. Balding DPCs secreted higher levels of the negative hair growth regulators transforming growth factor beta 1 and 2 in response to H2O2 but not cell culture-associated oxidative stress. Balding DPCs had higher levels of catalase and total glutathione but appear to be less able to handle oxidative stress compared with occipital DPCs. These in vitro findings suggest that there may be a role for oxidative stress in the pathogenesis of AGA both in relation to cell senescence and migration but also secretion of known hair follicle inhibitory factors.
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Increased oxidative stress and mitochondrial stress are implicated in causing androgenetic alopecia.
“Increased oxidative stress and mitochondrial stress were implicated in causing androgenetic alopecia (permanent hair loss) (Ho et al., 2019; Upton et al., 2015).”
From Comprehensive Multi-omics Analysis Reveals Mitochondrial Stress as a Central Biological Hub for Spaceflight Impact (2020) · cites this paper as Upton et al., 2015
The Abstract (page unavailable) says the in vitro findings suggest a role for oxidative stress in the pathogenesis of androgenetic alopecia. The paper does not identify mitochondrial stress as a contributor, and its evidence suggests a possible role rather than establishing that oxidative stress causes the condition. (LLM, conf=0.87)
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“Increased oxidative stress and mitochondrial stress were implicated in causing androgenetic alopecia (permanent hair loss) (Ho et al., 2019; Upton et al., 2015).”
BackgroundFocus on the Contribution of Oxidative Stress in Skin Aging
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- Authors
- Upton, J. H., Hannen, R. F., Bahta, A. W., Farjo, N., Farjo, B., & Philpott, M. P.
- Affiliations
- Queen Mary University of London (GB)
- Corresponding author
- Philpott, Michael P.
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2015-05
- Volume
- 135
- Issue
- 5
- Pages
- 1244-1252
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W1979998542
- Cited by
- 233
- References
- 56
- Citations by year
- 2026: 33 · 2025: 38 · 2024: 30 · 2023: 27 · 2022: 19 · 2021: 28 · 2020: 24 · 2019: 9 · 2018: 7 · 2017: 8 · 2016: 9 · 2013: 1
- FWCI
- 10.31
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Funders
- Biotechnology and Biological Sciences Research Council
- Topics
- Health Sciences › Medicine › Urology › Hair Growth and Disorders
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Keywords
- androgenetic alopecia, dermal papilla cells, premature senescence, oxidative stress, p16INK4a, reactive oxygen species, hydrogen peroxide, TGF-β1, TGF-beta2, catalase, glutathione, hair follicle, cell migration
- MeSH terms
- Adult, Alopecia, Biopsy, Needle, Catalase, Cell Movement, Cells, Cultured, Glutathione, Humans, Male, Middle Aged, Oxygen, Scalp, Case-Control Studies, Cellular Senescence, Reactive Oxygen Species, Oxidative Stress, Cyclin-Dependent Kinase Inhibitor p16, Dermis, In Vitro Techniques
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