Expression of nitric oxide synthases in keratinocytes after UVB irradiation

Chang, Huoy-Rou; Tsao, Der-An; Wang, Shiow-Ru; Yu, Hsin‐Su

doi:10.1007/s00403-003-0433-4

Cited by 47 publications

(31 citation statements)

References 24 publications

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“…UVR induces production of reactive nitrogen species, including NO, and reactive oxygen species, including superoxide radicals, in skin cells (Deliconstantinos et al, 1996;Bruch-Gerharz et al, 1998;Chang et al, 2003;Aitken et al, 2007). Although NO is increased within minutes after UVR treatment in HaCaT cells, these are not primary keratinocytes (Aitken et al, 2007).…”

Section: Discussionmentioning

confidence: 94%

Opening of Chloride Channels by 1α,25-Dihydroxyvitamin D 3 Contributes to Photoprotection against UVR-Induced Thymine Dimers in Keratinocytes

Sequeira

Rybchyn

Gordon-Thomson

et al. 2013

Journal of Investigative Dermatology

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UVR produces vitamin D in skin, which is hydroxylated locally to 1α,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)). 1,25(OH)(2)D(3) protects skin cells against UVR-induced DNA damage, including thymine dimers, but the mechanism is unknown. As DNA repair is inhibited by nitric oxide (NO) products but facilitated by p53, we examined whether 1,25(OH)(2)D(3) altered the expression of nitrotyrosine, a product of NO, or p53 after UVR in human keratinocytes. 1,25(OH)(2)D(3) and the nongenomic agonist 1α,25-dihydroxylumisterol(3) reduced nitrotyrosine 16 hours after UVR, detected by a sensitive whole-cell ELISA. p53 was enhanced after UVR, and this was further augmented in the presence of 1,25(OH)(2)D(3). DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid), a chloride channel blocker previously shown to prevent 1,25(OH)(2)D(3)-induced chloride currents in osteoblasts, had no effect on thymine dimers on its own but prevented the 1,25(OH)(2)D(3)-induced protection against thymine dimers. Independent treatment with DIDS, at concentrations that had no effect on thymine dimers, blocked UVR-induced upregulation of p53. In contrast, reduction of nitrotyrosine remained in keratinocytes treated with 1,25(OH)(2)D(3) and DIDS at concentrations shown to block decreases in post-UVR thymine dimers. These results suggest that 1,25(OH)(2)D(3)-induced chloride currents help protect from UVR-induced thymine dimers, but further increases in p53 or reductions of nitrotyrosine by 1,25(OH)(2)D(3) are unlikely to contribute substantially to this protection.

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Section: Discussionmentioning

confidence: 94%

Opening of Chloride Channels by 1α,25-Dihydroxyvitamin D 3 Contributes to Photoprotection against UVR-Induced Thymine Dimers in Keratinocytes

Sequeira

Rybchyn

Gordon-Thomson

et al. 2013

Journal of Investigative Dermatology

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“…Further pathways include immune-related functions (e.g., B cell receptor signaling pathway, fMLP-induced chemokine gene expression in HMC-1 cells, and MEF2D in T cell apoptosis) and, interestingly, the nitric oxide signaling pathway. Of note, nitric oxide plays diverse biological functions, and in the skin, it is involved in the maintenance of barrier function, melanogenesis, erythema, immunosuppression, and the protection of keratinocytes against UV-induced apoptosis [31, 32]. On the other hand, the biological process analysis reveals phosphate ion metabolism as the most enriched term.…”

Section: Resultsmentioning

confidence: 99%

Improved detection of gene-microbe interactions in the mouse skin microbiota using high-resolution QTL mapping of 16S rRNA transcripts

et al. 2017

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BackgroundRecent studies highlight the utility of quantitative trait locus (QTL) mapping for determining the contribution of host genetics to interindividual variation in the microbiota. We previously demonstrated that similar to the gut microbiota, abundances of bacterial taxa in the skin are significantly influenced by host genetic variation. In this study, we analyzed the skin microbiota of mice from the 15th generation of an advanced intercross line using a novel approach of extending bacterial trait mapping to both the 16S rRNA gene copy (DNA) and transcript (RNA) levels, which reflect relative bacterial cell number and activity, respectively.ResultsRemarkably, the combination of highly recombined individuals and 53,203 informative SNPs allowed the identification of genomic intervals as small as <0.1 megabases containing single genes. Furthermore, the inclusion of 16S rRNA transcript-level mapping dramatically increased the number of significant associations detected, with five versus 21 significant SNP-bacterial trait associations based on DNA- compared to RNA-level profiling, respectively. Importantly, the genomic intervals identified contain many genes involved in skin inflammation and cancer and are further supported by the bacterial traits they influence, which in some cases have known genotoxic or probiotic capabilities.ConclusionsThese results indicate that profiling based on the relative activity levels of bacterial community members greatly enhances the capability of detecting interactions between the host and its associated microbes. Finally, the identification of several genes involved in skin cancer suggests that similar to colon carcinogenesis, the resident microbiota may play a role in skin cancer susceptibility and its potential prevention and/or treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s40168-017-0275-5) contains supplementary material, which is available to authorized users.

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“…Higher levels of NOS activity, stimulated by UV radiation, initiate other more complex reactions that include various cell types. The NO liberated following UV radiation plays a significant role in initiating melanogenesis, erythema, and immunosuppression 41,42 .…”

Section: Nitric Oxide Synthasementioning

confidence: 99%