Role of the aryl hydrocarbon receptor in tobacco smoke extract–induced matrix metalloproteinase‐1 expression
Abstract
Findings from large epidemiologic studies indicate that there is a link between smoking and extrinsic skin ageing. We previously reported that matrix metalloproteinases (MMP s) mediate connective tissue damage in skin exposed to tobacco smoke extracts. Tobacco smoke contains more than 3800 constituents, including numerous water‐insoluble polycyclic aromatic hydrocarbons (PAH s) that trigger aryl hydrocarbon receptor (A h R) signalling pathways. To analyse the molecular mechanisms involved in tobacco smoke–induced skin ageing, we exposed primary human fibroblasts and keratinocytes to tobacco smoke extracts. Hexane‐ and water‐soluble tobacco smoke extracts significantly induced MMP‐1 m RNA in both human cultured fibroblasts and keratinocytes in a dose‐dependent manner. To clarify the involvement of the A h R pathway, we used a stable A h R‐knockdown H a C a T cell line. A h R knockdown abolished the increased transcription of the A h R‐dependent genes CYP 1 A 1/CYP 1 B 1 and MMP‐1 induced by either of the tobacco smoke extracts. Furthermore, the tobacco smoke extracts induced 7‐ethoxyresorufin‐O‐deethylase activity, which was almost completely abolished by A h R knockdown. Likewise, treating fibroblasts with A h R pathway inhibitors, that is, the flavonoids 3‐methoxy‐4‐nitroflavone and α‐naphthoflavone, blocked the expression of CYP 1 B 1 and MMP‐1. These findings suggest that the tobacco smoke extracts induce MMP‐1 expression in human fibroblasts and keratinocytes via activation of the A h R pathway. Thus, the A h R pathway may be pathogenetically involved in extrinsic skin ageing.
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AHR activation and increased CYP1A1 expression have also been reported after exposure to B[a]P, PM2.5 and water-soluble tobacco smoke extracts.
“AHR activation and increased CYP1A1 expression have also been reported after exposure to B[a]P,38 PM2.5 39 and water‐soluble tobacco smoke extracts.40”
From The impact of airborne pollution on skin (2019) · cites this paper as [40]
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Self-citation
- Authors
- Ono, Y., Torii, K., Fritsche, E., Shintani, Y., Nishida, E., Nakamura, M., Shirakata, Y., Haarmann‐Stemmann, T., Abel, J., Krutmann, J., & Morita, A.
- Affiliations
- Nagoya City University (JP)
- Leibniz Institute of Environmental Medicine (DE)
- Ehime University (JP)
- Corresponding author
- Morita, Akimichi
- ORCID
- Venue
- Experimental Dermatology
- Publisher
- Wiley
- Published
- 2013-04-25
- Volume
- 22
- Issue
- 5
- Pages
- 349-353
- ISSN
- 0906-6705 (ISSN-L)
- 1600-0625
- OpenAlex
- W2070732234
- Cited by
- 87
- References
- 27
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 5 · 2023: 10 · 2022: 8 · 2021: 10 · 2020: 5 · 2019: 8 · 2018: 5 · 2017: 2 · 2016: 13 · 2015: 6 · 2014: 6 · 2013: 2
- FWCI
- 10.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (25461707)
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Keywords
- aryl hydrocarbon receptor, MMP-1, polycyclic aromatic hydrocarbons, CYP1A1, CYP1B1, HaCaT keratinocytes, fibroblasts, ethoxyresorufin-O-deethylase, flavonoid inhibitors, alpha-naphthoflavone, connective tissue damage
- MeSH terms
- Aryl Hydrocarbon Hydroxylases, Cell Line, Cells, Cultured, Fibroblasts, Hexanes, Humans, Solubility, Tobacco Smoke Pollution, Signal Transduction, Skin Aging, Keratinocytes, Receptors, Aryl Hydrocarbon, Oxidative Stress, Cytochrome P-450 CYP1A1, Matrix Metalloproteinase 1, Cytochrome P-450 CYP1B1
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