Cited by 43Redox biology and oxidative stressSkin Protection and AgingEffects of Radiation Exposure

Protective Role of Mitochondrial Peroxiredoxin III against UVB-Induced Apoptosis of Epidermal Keratinocytes

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Baek, Jin Young, Park, Sujin, Park, Jiyoung, Jang, Ji Yong, Wang, Su Bin, Kim, Sin Ri, Woo, Hyun Ae, Lim, Kyung Min +1 more·2017·Journal of Investigative Dermatology

Abstract

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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Crossref · 10.1016/j.jid.2017.01.027

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Cited works that were retracted

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  • Cites a retracted work: 10.1016/s0014-5793(03)00238-2

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    The cited work was retracted on 2025-02-26 (notice 10.1002/1873-3468.70019), not before this paper was published (2017-06).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

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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
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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