Cited by 21Epigenetics and DNA MethylationSkin Protection and AgingTGF-β signaling in diseases

Inhibition of DNA methylation in the COL1A2 promoter by anacardic acid prevents UV-Induced decrease of type i procollagen expression

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Kim, Min-Kyoung, Kim, Eun Ju, Cheng, Yao, Shin, Mi Hee, Oh, Jang-Hee, Lee, Dong Hun, Chung, Jin Ho·2017·Journal of Investigative Dermatology

Abstract

UV radiation decreases type I procollagen production mainly by inhibiting the transforming growth factor-β/Smad signaling pathway. Because further epigenetic regulatory mechanisms are unclear, we investigated the roles of DNA methylation and histone acetylation in UV-induced regulation of COL1A2 transcription in human dermal fibroblasts. Anacardic acid, a p300 histone acetyltransferase inhibitor, rescued the UV-induced decrease of type I procollagen expression in human dermal fibroblasts. Although UV irradiation induced global histone acetylation, it reduced the local recruitment of histone H3 acetylation as well as p300, and Smad2/3 to the p300 binding site (-1406/-1393), in the COL1A2 promoter as shown by chromatin immunoprecipitation. This effect was reversed by anacardic acid treatment. In contrast, pyrosequencing analysis showed that UV irradiation induced DNA methylation in the same region of the COL1A2 promoter, which was reversed by anacardic acid and a DNA methyltransferase inhibitor (5-AZA-2'-deoxycytidine). Inhibition of UV-induced DNA methylation led to an increase of UV-induced histone acetylation in the COL1A2 promoter and increased the recruitment of transcription factors, leading to up-regulation of type I collagen after UV irradiation. Collectively, our findings indicate that the epigenetic crosstalk between DNA methylation and histone acetylation plays a crucial role in COL1A2 transcription induced by UV irradiation.

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Crossref · 10.1016/j.jid.2017.02.005

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  • UV radiation decreases type I procollagen production mainly by inhibiting the TGF-β/Smad signaling pathway.

    “UV radiation decreases type I procollagen production mainly by inhibiting the TGF-β/Smad signaling pathway [43].”

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Authors
Kim, M.-K., Kim, E. J., Cheng, Y., Shin, M. H., Oh, J.-H., Lee, D. H., & Chung, J. H.
Affiliations
Seoul National University (KR)
Corresponding author
  • Lee, Dong Hun
  • Chung, Jin Ho
Venue
Journal of Investigative Dermatology
Publisher
Elsevier BV
Published
2017-06
Volume
137
Issue
6
Pages
1343-1352
ISSN
0022-202X (ISSN-L)
OpenAlex
W2590952606
Cited by
21
References
45
Citations by year
2026: 4 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 4 · 2020: 1 · 2019: 1 · 2018: 4
FWCI
0.67
Type
journal article
Language
en
Open access
Locations
  • Journal of Investigative Dermatology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
  • Health Sciences › Medicine › Dermatology › Skin Protection and Aging
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Keywords
anacardic acid, DNA methylation, histone acetylation, type I procollagen, ultraviolet radiation, P300, histone H3 acetylation, Smad2/3, epigenetic regulation, dermal fibroblasts, decitabine, epigenetic crosstalk
MeSH terms
Acetylation, Cells, Cultured, DNA-Binding Proteins, Fibroblasts, Histones, Humans, Promoter Regions, Genetic, Ultraviolet Rays, Transcriptional Activation, Up-Regulation, DNA Methylation, Collagen Type I, Chromatin Immunoprecipitation, Anacardic Acids, E1A-Associated p300 Protein

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