Silver ions enhance UVB‐induced phosphorylation of histone H2AX

Zhao, Xiaoxu; Toyooka, Tatsushi; Ibuki, Yuko

doi:10.1002/em.21875

Cited by 14 publications

(10 citation statements)

References 47 publications

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“…The induction of this marker of oxidative stress and DNA damage by silver was described in vivo 28,29 and in vitro 30 . Zhao et al observed in vitro that the amount of γH2AX was directly proportional to the silver dose 31 . In our ex vivo experiment, the silver dressings caused an increase in γH2AX (Fig.…”

Section: Discussionmentioning

confidence: 99%

Effects of wound dressings containing silver on skin and immune cells

Nešporová

Pavlík

Šafránková

et al. 2020

Sci Rep

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Wound dressings with silver have been shown to be cytotoxic in vitro. However, the extrapolation of this cytotoxicity to clinical settings is unclear. We applied dressings with various forms of silver on porcine skin ex vivo and investigated silver penetration and DNA damage. We assessed antimicrobial efficacy, cytotoxicity to skin cells, and immune response induced by the dressings. All dressings elevated the DNA damage marker γ-H2AX and the expression of stress-related genes in explanted skin relative to control. This corresponded with the amount of silver in the skin. The dressings reduced viability, induced oxidative stress and DNA damage in skin cells, and induced the production of pro-inflammatory IL-6 by monocytes. The oxidative burst and viability of activated neutrophils decreased. The amount of silver released into the culture medium varied among the dressings and correlated with in vitro toxicity. However, antimicrobial efficiencies did not correlate strongly with the amount of silver released from the dressings. Antimicrobial efficiency and toxicity are driven by the form of silver and the construction of dressings and not only by the silver concentration. The damaging effects of silver dressings in ex vivo skin highlight the importance of thorough in vivo investigation of silver dressing toxicity.

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Section: Discussionmentioning

confidence: 99%

Effects of wound dressings containing silver on skin and immune cells

Nešporová

Pavlík

Šafránková

et al. 2020

Sci Rep

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“…Most genotoxins induce foci only as secondary events, when unrepaired DNA lesions cause replication forks to stall and/or collapse in cells passing through S phase following exposure. Consistent with this notion, foci induction has been reported to be delayed, peaking only several hours after exposure to agents such as UV light and alkylating agents [Staszewski et al, ; Zhao et al, ] and not always showing the distinct pattern of individual spots seen for ionizing radiation‐induced DNA damage foci, but instead sometimes a more homogenous, pan‐nuclear signal (see e.g. Fig.…”

Section: Dna Double‐strand Breaksmentioning

confidence: 70%

DNA damage foci: Meaning and significance

Rothkamm

Barnard

Moquet

et al. 2015

Environ and Mol Mutagen

289

228

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The discovery of DNA damage response proteins such as γH2AX, ATM, 53BP1, RAD51, and the MRE11/RAD50/NBS1 complex, that accumulate and/or are modified in the vicinity of a chromosomal DNA double-strand break to form microscopically visible, subnuclear foci, has revolutionized the detection of these lesions and has enabled studies of the cellular machinery that contributes to their repair. Double-strand breaks are induced directly by a number of physical and chemical agents, including ionizing radiation and radiomimetic drugs, but can also arise as secondary lesions during replication and DNA repair following exposure to a wide range of genotoxins. Here we aim to review the biological meaning and significance of DNA damage foci, looking specifically at a range of different settings in which such markers of DNA damage and repair are being studied and interpreted.

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“…All graphical data are the means ± SD from three independent experiments, "#" and "##" indicate significantly different from the untreated control group at the p < 0.05 and p < 0.01 levels, respectively, "*" and "**" indicate significantly different from the UVB only control group at the p < 0.05 and p < 0.01 levels, respectively. important biomarker of DNA damage, but is also an important marker of apoptosis (Zhao et al, 2014;Huang et al, 2003). KGF-2 also decreased the formation of CPD and γ-H2AX in HEE and HaCaT cell (Figures 1C, 2D), indicating that KGF-2 could protect the epidermis from UVB induced DNA damage.…”

Section: Discussionmentioning

confidence: 89%

Keratinocyte Growth Factor 2 Ameliorates UVB-Induced Skin Damage via Activating the AhR/Nrf2 Signaling Pathway

et al. 2021

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Objective: Exposure to ultraviolet B (UVB) can cause skin damage through oxidative stress, DNA damage, and apoptosis. Keratinocyte growth factor (KGF) has been shown to reduce the content of intracellular reactive oxygen species (ROS) following UVB exposure, a role that is crucial for the efficient photoprotection of skin. The present study evaluated the photoprotective effect of KGF-2 on UVB-induced skin damage and explored its potential molecular mechanism.Methods: To evaluate the effect of KGF-2 on UVB-induced damage ex vivo, a human epidermal full-thickness skin equivalent was pretreated without or with KGF-2 and then exposed to UVB and the levels of histopathological changes, DNA damage, inflammation, and apoptosis were then evaluated. The ability of KGF-2 to protect the cells against UVB-inflicted damage and its effect on ROS production, apoptosis, and mitochondrial dysfunction were determined in HaCaT cells.Results: Pretreatment of the epidermis with KGF-2 ameliorated the extent of photodamage. At the cellular level, KGF-2 could attenuate ROS production, apoptosis, DNA damage, and mitochondrial dysfunction caused by UVB exposure. KGF-2 could also activate the aryl hydrocarbon receptor (AhR) to trigger the Nrf2 signaling pathway.Conclusion: Taken together, our findings suggested that KGF-2 could ameliorate UVB-induced skin damage through inhibiting apoptosis, reducing oxidative stress, and preventing DNA damage and mitochondrial dysfunction via regulating AhR/Nrf2 signaling pathway.

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Silver ions enhance UVB‐induced phosphorylation of histone H2AX

Cited by 14 publications

References 47 publications

Effects of wound dressings containing silver on skin and immune cells

Effects of wound dressings containing silver on skin and immune cells

DNA damage foci: Meaning and significance

Keratinocyte Growth Factor 2 Ameliorates UVB-Induced Skin Damage via Activating the AhR/Nrf2 Signaling Pathway

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