Different biological effects of a constant dose for single <scp>UVB</scp> irradiation with different intensities and exposure times

Iida, Machiko; Nakano, Chihiro; Tamaki, Marie; Hasegawa, Mari; Tsuzuki, Toyonori; Kato, Masashi

doi:10.1111/exd.12969

Cited by 10 publications

(10 citation statements)

References 8 publications

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“…These results corroborated with previous report by Novak et al 31. using in vitro model evaluating UVB-induced T-Cell apoptosis, and very recently Iida et al 17. also reported similar finding using C3H/HeNJcl mice.…”

Section: Discussionsupporting

confidence: 92%

“…These results provided a reasonable rationale explaining the increased proportion of keratinocytes harboring mutant p53 in the epidermis of normal appearing skin of mice receiving LI UVB radiation as compared to their HI UVB treated counterpart. Collaborating with our result, it was recently demonstrated that at equivalent exposure dose, single LI UVB treatment induced higher levels of 8-hydroxy-2′deoxy-guanosine expression, a recognized biomarker for DNA damage and oxidative stress, in the epidermis of hairless mice as compared to their HI UVB treated counterpart17. Taken together, these events contributed to enhanced UVB-induced photocarcinogenesis resulting from LI UVB radiation as compared to its HI counterpart when equivalent surface exposure was administered.…”

Section: Discussionsupporting

confidence: 88%

“…Erythema is the observed sunburn at moderate doses. It has demonstrated that UVB-induced erythema depends on surface exposure delivered regardless of irradiance171819. This phenomenon allowed us to examine the damaging effects of UVB radiation (same surface exposure) on the skin with different irradiance in a laboratory setting using a neutral density physical filter (a filter that does not change the spectrum) that avoids aforementioned potential confounders in animal studies using sunscreen to reduce irradiance.…”

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confidence: 99%

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Irradiance-dependent UVB Photocarcinogenesis

Lan

Huang

et al. 2016

Sci Rep

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Ultraviolet B (UVB) radiation from the sun may lead to photocarcinogenesis of the skin. Sunscreens were used to protect the skin by reducing UVB irradiance, but sunscreen use did not reduce sunburn episodes. It was shown that UVB-induced erythema depends on surface exposure but not irradiance of UVB. We previously showed that irradiance plays a critical role in UVB-induced cell differentiation. This study investigated the impact of irradiance on UVB-induced photocarcinogenesis. For hairless mice receiving equivalent exposure of UVB radiation, the low irradiance (LI) UVB treated mice showed more rapid tumor development, larger tumor burden, and more keratinocytes harboring mutant p53 in the epidermis as compared to their high irradiance (HI) UVB treated counterpart. Mechanistically, using cell models, we demonstrated that LI UVB radiation allowed more keratinocytes harboring DNA damages to enter cell cycle via ERK-related signaling as compared to its HI UVB counterpart. These results indicated that at equivalent exposure, UVB radiation at LI has higher photocarcinogenic potential as compared to its HI counterpart. Since erythema is the observed sunburn at moderate doses and use of sunscreen was not found to associate with reduced sunburn episodes, the biological significance of sunburn with or without sunscreen use warrants further investigation.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 88%

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confidence: 99%

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Irradiance-dependent UVB Photocarcinogenesis

Lan

Huang

et al. 2016

Sci Rep

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“…In the context of biostimulation, using primitive pigment cell development as a model for investigation, we had shown that after equivalent fluence, high irradiance UVB (HIUVB) emitted from excimer light device contributes to more effective vitiligo repigmentation clinically by inducing more efficient pigment cell differentiation via aryl hydrocarbon receptor (AhR)-related pathway as compared to its low irradiance UVB (LIUVB) counterpart [3]. In terms of cutaneous immune suppression, it has been demonstrated that HIUVB suppresses cutaneous immunity more effectively as compare to its LIUVB counterpart after equal fluence exposure using contact hypersensitivity (CHS) animal models, although the mechanism involved remains unexplored [4,5].…”

Section: Introductionmentioning

confidence: 99%

The impact of irradiance on UVB-induced cutaneous immunosuppression: Implications on administering most efficient phototherapy

Lai

Lin

et al. 2019

Journal of Dermatological Science

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A B S T R A C TBackground: Ultraviolet B (UVB) is commonly used for treating dermatologic conditions. Recently, high irradiance UVB (HIUVB) has been suggested to be more effective for treating skin conditions as compared to its low irradiance (LI) counterpart. The biological impact of UVB radiation emitted at different irradiance on cutaneous immunity remains obscure.Objective: This study aimed to explore the impacts of UVB radiation administered at equivalent fluence (mJ/cm 2 ) but different irradiance (mW/cm 2 ) on cutaneous immune response. Methods: Cultured bone marrow derived dendritic cell (BMDC) were treated with equivalent fluence of UVB radiation with HIUVB or LIUVB. The phenotypic and functional alterations of BMDCs were documented. Animal models were used to validate the in vitro results in vivo and explore the mechanisms involved. Results: After equivalent fluence of UVB radiation, the HIUVB treated BMDC showed significantly lower MHCII and CD86 expressions, reduced capacity to stimulate T cell proliferation, and enhanced activation of aryl hydrocarbon receptor (AhR)-activated genes as compared to control while their LIUVB treated counterpart showed no significant change. Using animal model, the HIUVB induced significantly higher immune suppressive effect in mice as compared to their LIUVB counterpart after equivalent fluence of UVB treatment. The superior immune suppressive effect of HIUVB over LIUVB radiation was not observed when similar experiments were performed using AhR-deficient mice. Conclusion: We propose irradiance played an important role modulating UVB-induced cutaneous immune suppression. Future works on UVB phototherapy, both clinical and research, should incorporate this important parameter into consideration.

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“…There is in vivo evidence that less intense exposures may be more important for skin cancer induction than more intense doses which cause more apoptosis (8), and even for a single exposure there are significant differences in skin responses between the same dose (i.e. the same levels of DNA damage) administered with high intensity over a short period versus a low intensity for a longer period (9). Our skin can protect itself via pigmentation responses (tanning), but also by "photo-adaption", which is independent of pigmentation levels (10).…”

Section: Introductionmentioning

confidence: 99%

Different genetic mechanisms mediate spontaneous versus UVR-induced malignant melanoma

Walker

Ferguson

Handoko

et al. 2018

Preprint

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wordsGenetic variation conferring resistance and susceptibility to carcinogen-induced tumorigenesis is frequently studied in mice. We have now turned this to melanoma using the collaborative cross (CC), a resource of mouse strains designed to discover genes for complex diseases. We studied melanomaprone transgenic progeny across seventy CC genetic backgrounds. We mapped a strong quantitative trait locus for rapid onset spontaneous melanoma onset to Prkdc, a gene involved in detection and repair of DNA damage. In contrast, rapid onset UVR-induced melanoma was linked to the ribosomal subunit gene Rrp15. Ribosome biogenesis was upregulated in skin shortly after UVR exposure, Mechanistically, variation in the "usual suspects" by which UVR may exacerbate melanoma, defective DNA repair, melanocyte proliferation, or inflammatory cell infiltration, did not explain melanoma susceptibility or resistance across the CC. Instead, events occurring soon after exposure, such as dysregulation of ribosome function, which alters many aspects of cellular metabolism, may be important.neutrophil monoclonal antibody Abcam ab2557: NIMP-R14 (Cambridge, UK) at a concentration of 1:100. Neutrophil depletion:Each NOD/Cdk4 R24C/+ ::NRAS pup was injected intraperitoneally, with either 100ug InVivo MAb antimouse Ly6G (Bio C Cell, Beverly, MA, USA) or PBS (as a control) at P2, P3 and P5. At P3, all pups were also given UVR treatment. As the depletion was done using anti-Ly6G, staining to differentiate between depleted and non-depleted skin was done using Myeloperoxidase staining (Abnova rabbit anti-MPO, Taipei, Taiwan) at a concentration of 1:75. Statistical Analysis:One-way Anova tests were used to determine the significant difference between means, using R. The survival of mice in each treatment group was estimated using Kaplan-Meier analysis (PRISM TM ), and the Log-Rank (Mantel-Cox) test was used to test for differences between the groups. For correlation comparisons Pearson correlation r value was calculated in PRISM along with the p-value for significant correlation.

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Different biological effects of a constant dose for single UVB irradiation with different intensities and exposure times

Cited by 10 publications

References 8 publications

Irradiance-dependent UVB Photocarcinogenesis

Irradiance-dependent UVB Photocarcinogenesis

The impact of irradiance on UVB-induced cutaneous immunosuppression: Implications on administering most efficient phototherapy

Different genetic mechanisms mediate spontaneous versus UVR-induced malignant melanoma

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