Circular RNA (circRNA) is a class of noncoding RNA that regulates the activity of microRNAs and gene expression. Altered circRNA expression is associated with human diseases. The present study profiled differentially expressed circRNAs in the ultraviolet B stress‐induced human fibroblast premature senescence (UVB‐SIPS) model, and assessed the role of circRNA_100797 in UVB‐SIPS. The UVB‐SIPS model was confirmed by ß‐galactosidase staining, cell viability CCK‐8 assay, and flow cytometric cell cycle distribution assay, and subjected to circRNA gene chip profiling. These differentially expressed circRNAs were analyzed using the clusterProfiler R package for Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) database pathways. The selected circRNAs were confirmed using quantitative reverse transcription polymerase chain reaction (qRT‐PCR), the relationship of circRNA_100797 with miR‐23a‐5p was assessed using luciferase reporter assay, and their functions were determined by qRT‐PCR and western blot analysis. A total of 472 differentially expressed circRNAs occurred in the UVB‐SIPS. qRT‐PCR confirmed five of eight differentially expressed circRNAs. The GO and KEGG analyses revealed that these differently expressed circRNAs function in biology process, cell component, and molecular function. Furthermore, it was found that circRNA_100797 had a low expression in UVB‐SIPS. However, when circRNA_100797 was overexpressed, the acceleration of cell proliferation and alleviation of cell cycle arrest were observed. Moreover, circRNA_100797 could target miR‐23a‐5p, their expression levels were inversely associated in fibroblasts, and the miR‐23a‐5p overexpression blocked the effect of the overexpression of circRNA_100797 in UVB‐SIPS. The present study demonstrated that circRNA_100797 acts as a sponge of miR‐23a‐5p, and has a photoprotection role in UVB‐irradiated fibroblasts.

Exosomal microRNAs have been investigated in bystander effect, but it is unclear whether microRNA works in ultraviolet radiation–induced bystander effects (UV-RIBEs) and what the underlying mechanism could be. Exosomes from ultraviolet (UV)–irradiated human skin fibroblasts (HSFs) were isolated and transferred to normal HSFs, followed by the detection of proliferation rate, oxidative damage level, and apoptosis rate. Exosomal miRNAs were evaluated and screened with miRNA sequencing and quantitative reverse transcriptase–polymerase chain reaction method. MiRNA shuttle and bystander photodamage reactions were observed after transfection of miR-769-5p. MiR-769-5p targeting gene transforming growth factor-β1 (TGFBR1), and TGFBR1 mRNA 3′-untranslated region (UTR) was assessed and identified by Western blotting and dual-luciferase reporter assay. Bystander effects were induced after being treated with isolated exosomes from UV-irradiated HSFs. Exosomal miR-769-5p expression was significantly upregulated. Human skin fibroblasts showed lower proliferation, increasing oxidative damage, and faster occurrence of apoptosis after transfection. Exosome-mediated transfer of miR-769-5p was observed. Upregulation of miR-769-5p induced bystander effects, whereas downregulation of miR-769-5p can suppress UV-RIBEs. In addition, miR-769-5p was found to downregulate TGFBR1 gene expression by directly targeting its 3′-UTR. Our results demonstrate that exosome-mediated miR-769-5p transfer could function as an intercellular messenger and exacerbate UV-RIBEs. MiR-769-5p inhibits the expression of TGFBR1 by targeting TGFBR1 mRNA 3′-UTR.

Aim To determine whether 5-aminolevulinic acid-based photodynamic therapy (ALA-PDT) is effective in combating ultraviolet A- (UVA-) induced oxidative photodamage of hairless mice skin in vivo and human epidermal keratinocytes in vitro. Methods In in vitro experiments, the human keratinocyte cell line (HaCaT cells) was divided into two groups: the experimental group was treated with ALA-PDT and the control group was left untreated. Then, the experimental group and the control group of cells were exposed to 10 J/m2 of UVA radiation. ROS, O2− species, and MMP were determined by fluorescence microscopy; p53, OGG1, and XPC were determined by Western blot analysis; apoptosis was determined by flow cytometry; and 8-oxo-dG was determined by immunofluorescence. Moreover, HaCaT cells were also treated with ALA-PDT. Then, SOD1 and SOD2 were examined by Western blot analysis. In in vivo experiments, the dorsal skin of hairless mice was treated with ALA-PDT or saline-PDT, and then, they were exposed to 20 J/m2 UVA light. The compound 8-oxo-dG was detected by immunofluorescence. Conclusion In human epidermal keratinocytes and hairless mice skin, UVA-induced oxidative damage can be prevented effectively with ALA-PDT pretreatment.