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Network analysis to understand side effects of UVB on skin through transcriptomic approach

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A Correction to this article was published on 27 June 2022

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Abstract

Background

Ultraviolet B (UVB) light can exert toxic effects on the skin by penetrating the epidermal layer and exposing the skin cells, potentially leading to skin disease. Although epidemiological studies have reported associations between UVB and the pathogenesis of skin diseases, few studies have focused on elucidating the underlying mechanisms of skin damage induced by UVB through biological network analysis.

Objective

The present study aimed to explore the potential mechanisms of the toxic effects of UVB on skin and suggested biomarkers by analyzing a signaling network by UVB radiation through a transcriptomic approach.

Results

Through a literature-based network analysis, the oxidative stress and inflammatory response were predicted as major UVB-induced signaling alterations in keratinocytes. UVB light might cause skin cancer, including melanoma and squamous cell carcinoma, through the accumulation of DNA damage and oxidative stress induced by expression changes incorporating CDKN1A, FAS, FOS, MDM2, PLAUR, and TNF.

Conclusion

The analytical approach used in this study suggests that the regulation of gene expression by UVB light leads to skin diseases by changing the cellular processes of keratinocytes. This strategy can be applied to research to suggest mechanisms and biomarkers from a toxicological perspective. Although further functional studies on the modes of action for each factor are required, this study might help develop strategies for exploring UVB light-induced signaling networks through analyzing transcriptomic data.

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References

  • Addison R et al (2021) Therapeutic wavelengths of ultraviolet B radiation activate apoptotic, circadian rhythm, redox signalling and key canonical pathways in psoriatic epidermis. Redox Biol 41:101924

    Article  CAS  Google Scholar 

  • Bashir MM, Sharma MR, Werth VP (2009) TNF-alpha production in the skin. Arch Dermatol Res 301:87–91

    Article  CAS  Google Scholar 

  • Basset-Seguin N et al (1991) C-fos and c-jun proto-oncogene expression is decreased in psoriasis: an in situ quantitative analysis. J Invest Dermatol 97:672–678

    Article  CAS  Google Scholar 

  • Bruls WA, Slaper H, van der Leun JC, Berrens L (1984) Transmission of human epidermis and stratum corneum as a function of thickness in the ultraviolet and visible wavelengths. Photochem Photobiol 40:485–494

    Article  CAS  Google Scholar 

  • Casamassimi A, Federico A, Rienzo M, Esposito S, Ciccodicola A (2017) Transcriptome profiling in human diseases: new advances and perspectives. Int J Mol Sci 18:1652

    Article  Google Scholar 

  • Che X, Dai W (2019) Negative regulation of aryl hydrocarbon receptor by its lysine mutations and exposure to nickel. Mol Cell Toxicol 15:459–467

    Article  CAS  Google Scholar 

  • Chouinard N et al (2001) Repeated exposures of human skin equivalent to low doses of ultraviolet-B radiation lead to changes in cellular functions and accumulation of cyclobutane pyrimidine dimers. Biochem Cell Biol 79:507–515

    Article  CAS  Google Scholar 

  • Corley SM et al (2018) Plau and Tgfbr3 are YAP-regulated genes that promote keratinocyte proliferation. Cell Death Dis 9:1106

    Article  Google Scholar 

  • D’Orazio J, Jarrett S, Amaro-Ortiz A, Scott T (2013) UV radiation and the skin. Int J Mol Sci 14:12222–12248

    Article  Google Scholar 

  • Dutto I, Tillhon M, Cazzalini O, Stivala LA, Prosperi E (2015) Biology of the cell cycle inhibitor p21(CDKN1A): molecular mechanisms and relevance in chemical toxicology. Arch Toxicol 89:155–178

    Article  CAS  Google Scholar 

  • Elwood JM, Lee JA, Walter SD, Mo T, Green AE (1974) Relationship of melanoma and other skin cancer mortality to latitude and ultraviolet radiation in the United States and Canada. Int J Epidemiol 3:325–332

    Article  CAS  Google Scholar 

  • Esser C, Bargen I, Weighardt H, Haarmann-Stemmann T, Krutmann J (2013) Functions of the aryl hydrocarbon receptor in the skin. Semin Immunopathol 35:677–691

    Article  CAS  Google Scholar 

  • Fritsche E et al (2007) Lightening up the UV response by identification of the arylhydrocarbon receptor as a cytoplasmatic target for ultraviolet B radiation. Proc Natl Acad Sci USA 104:8851–8856

    Article  CAS  Google Scholar 

  • Golbeck J (2013) Analyzing the social web. Newnes

    Google Scholar 

  • Guinea-Viniegra J et al (2012) Differentiation-induced skin cancer suppression by FOS, p53, and TACE/ADAM17. J Clin Invest 122:2898–2910

    Article  CAS  Google Scholar 

  • Haarmann-Stemmann T, Esser C, Krutmann J (2015) The Janus-faced role of aryl hydrocarbon receptor signaling in the skin: consequences for prevention and treatment of skin disorders. J Invest Dermatol 135:2572–2576

    Article  CAS  Google Scholar 

  • Imokawa G (2009) Mechanism of UVB-induced wrinkling of the skin: paracrine cytokine linkage between keratinocytes and fibroblasts leading to the stimulation of elastase. J Investig Dermatol Symp Proc 14:36–43

    Article  CAS  Google Scholar 

  • Macleod KF et al (1995) p53-dependent and independent expression of p21 during cell growth, differentiation, and DNA damage. Genes Dev 9:935–944

    Article  CAS  Google Scholar 

  • Oishi M, Maeda K, Sugiyama S (1994) Distribution of apoptosis-mediating Fas antigen in human skin and effects of anti-Fas monoclonal antibody on human epidermal keratinocyte and squamous cell carcinoma cell lines. Arch Dermatol Res 286:396–407

    Article  CAS  Google Scholar 

  • Ozgur A, Vu T, Erkan G, Radev DR (2008) Identifying gene-disease associations using centrality on a literature mined gene-interaction network. Bioinformatics 24:i277-285

    Article  Google Scholar 

  • Palomo J, Dietrich D, Martin P, Palmer G, Gabay C (2015) The interleukin (IL)-1 cytokine family–balance between agonists and antagonists in inflammatory diseases. Cytokine 76:25–37

    Article  CAS  Google Scholar 

  • Rajabi P, Karimian P, Heidarpour M (2012) The relationship between MDM2 expression and tumor thickness and invasion in primary cutaneous malignant melanoma. J Res Med Sci 17:452–455

    CAS  PubMed  PubMed Central  Google Scholar 

  • Rundhaug JE, Fischer SM (2008) Cyclo-oxygenase-2 plays a critical role in UV-induced skin carcinogenesis. Photochem Photobiol 84:322–329

    Article  CAS  Google Scholar 

  • Subedi L, Lee TH, Wahedi HM, Baek SH, Kim SY (2017) Resveratrol-enriched rice attenuates UVB-ROS-induced skin aging via downregulation of inflammatory cascades. Oxid Med Cell Longev 2017:8379539

    Article  Google Scholar 

  • Takei K et al (2015) Cynaropicrin attenuates UVB-induced oxidative stress via the AhR-Nrf2-Nqo1 pathway. Toxicol Lett 234:74–80

    Article  CAS  Google Scholar 

  • Tanaka Y, Uchi H, Ito T, Furue M (2019) Indirubin-pregnane X receptor-JNK axis accelerates skin wound healing. Sci Rep 9:18174

    Article  CAS  Google Scholar 

  • Vierkotter A et al (2010) Airborne particle exposure and extrinsic skin aging. J Invest Dermatol 130:2719–2726

    Article  Google Scholar 

  • Wang Z, Gerstein M, Snyder M (2009) RNA-Seq: a revolutionary tool for transcriptomics. Nat Rev Genet 10:57–63

    Article  CAS  Google Scholar 

  • Yu S-L, Lee S-K (2017) Ultraviolet radiation: DNA damage, repair, and human disorders. Mol Cell Toxicol 13:21–28

    Article  CAS  Google Scholar 

  • Zhong W, Xing MM, Pan N, Maibach HI (2006) Textiles and human skin, microclimate, cutaneous reactions: an overview. Cutan Ocul Toxicol 25:23–39

    Article  CAS  Google Scholar 

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Acknowledgements

This study was supported by the grant from the Amorepacific Corporation R&I Center, Yongin, Republic of Korea.

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Authors and Affiliations

Authors

Contributions

YRS and HJK designed the research study. SJK, HWN and YJ performed overall experimental procedure and analyzed data. DYS reviewed the statistical analysis and also wrote the manuscript. HC reviewed and revised the manuscript.

Corresponding authors

Correspondence to Hyoung-June Kim or Young Rok Seo.

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Conflict of interests

Su Ji Kim, Hye-Won Na, Yujin Jang, Dong Yeop Shin, Hyunjung Choi, Hyoung-June Kim, Young Rok Seo declares that they have no conflict of interest.

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This article does not contain any studies with human participants or animals performed by any of the authors.

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The original online version of this article was revised: Due to an unfortunate oversight during the e.proofing process the article note has been given erroneously.

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Kim, S.J., Na, HW., Jang, Y. et al. Network analysis to understand side effects of UVB on skin through transcriptomic approach. Mol. Cell. Toxicol. 18, 457–467 (2022). https://doi.org/10.1007/s13273-021-00189-8

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