Protective Role of Mitochondrial Peroxiredoxin III against UVB-Induced Apoptosis of Epidermal Keratinocytes
Open accessAbstract
UVB light induces generation of reactive oxygen species, ultimately leading to skin cell damage. Mitochondria are a major source of reactive oxygen species in UVB-irradiated skin cells, with increased levels of mitochondrial reactive oxygen species having been implicated in keratinocyte apoptosis. Peroxiredoxin III (PrxIII) is the most abundant and potent H 2 O 2-removing enzyme in the mitochondria of most cell types. Here, the protective role of PrxIII against UVB-induced apoptosis of epidermal keratinocytes was investigated. Mitochondrial H 2 O 2 levels were differentiated from other types of ROS using mitochondria-specific fluorescent H 2 O 2 indicators. Upon UVB irradiation, PrxIII-knockdown HaCaT human keratinocytes and PrxIII-deficient (PrxIII-/-) mouse primary keratinocytes exhibited enhanced accumulation of mitochondrial H 2 O 2 compared with PrxIII-expressing controls. Keratinocytes lacking PrxIII were subsequently sensitized to apoptosis through mitochondrial membrane potential loss, cardiolipin oxidation, cytochrome c release, and caspase activation. Increased UVB-induced epidermal tissue damage in PrxIII-/- mice was attributable to increased caspase-dependent keratinocyte apoptosis. Our findings show that mitochondrial H 2 O 2 is a key mediator in UVB-induced apoptosis of keratinocytes and that PrxIII plays a critical role in protecting epidermal keratinocytes against UVB-induced apoptosis through eliminating mitochondrial H 2 O 2. These findings support the concept that reinforcing mitochondrial PrxIII defenses may help prevent UVB-induced skin damage such as inflammation, sunburn, and photoaging.
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Cites a retracted work: 10.1016/s0014-5793(03)00238-2
InfoThe cited work was retracted on 2025-02-26 (notice 10.1002/1873-3468.70019), not before this paper was published (2017-06).
Cited work 10.1016/s0014-5793(03)00238-2 · retracted 2025-02-26 · notice 10.1002/1873-3468.70019 · this paper published 2017-06
“Assefa, 2003, Ultraviolet B radiation-induced apoptosis in human keratinocytes: cytosolic activation of procaspase-8 and the role of Bcl-2, FEBS Lett, 540, 125, 10.1016/S0014-5793(03)00238-2”
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- Authors
- Baek, J. Y., Park, S., Park, J., Jang, J. Y., Wang, S. B., Kim, S. R., Woo, H. A., Lim, K. M., & Chang, T.-S.
- Affiliations
- Ewha Womans University (KR)
- Corresponding author
- Chang, Tong-Shin
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2017-06
- Volume
- 137
- Issue
- 6
- Pages
- 1333-1342
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W2588359075
- Cited by
- 43
- References
- 61
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 6 · 2023: 4 · 2022: 4 · 2021: 5 · 2020: 10 · 2019: 2 · 2018: 1 · 2017: 1
- FWCI
- 1.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- peroxiredoxin III, UVB-induced apoptosis, epidermal keratinocytes, mitochondrial hydrogen peroxide, reactive oxygen species, mitochondrial membrane potential, cardiolipin oxidation, cytochrome c release, caspase activation, photoaging, skin damage
- MeSH terms
- Epidermal Cells, Animals, Cell Survival, Cells, Cultured, Epidermis, Humans, Hydrogen Peroxide, Ultraviolet Rays, Keratinocytes, Apoptosis, Reactive Oxygen Species, Mice, Membrane Potential, Mitochondrial, Peroxiredoxin III
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