Role of the aryl hydrocarbon receptor in tobacco smoke extract–induced matrix metalloproteinase‐1 expression

Ono, Yuko; Torii, Kan; Fritsche, Ellen; Shintani, Yoichi; Nishida, Emi; Nakamura, Minoru; Shirakata, Yuji; Haarmann‐Stemmann, Thomas; Abel, Josef; Krutmann, Jean; Morita, Akimichi

doi:10.1111/exd.12148

Cited by 78 publications

(74 citation statements)

References 30 publications

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“…But the risk of side effects from erythema to severe skin damages like invasive squamous cell carcinomas limits long-term and child treatment (1)(2)(3)(4)(5). Blue light irradiation is an UV-free alternative, but the functional mechanisms of this treatment remain elusive (6)(7)(8)(9).…”

Section: Accepted For Publication 17 June 2013mentioning

confidence: 99%

“…Melanin pigmentation of the oral cavity is commonly observed among tobacco smokers, the so-called smoker's melanosis (2). Although many studies have shown that tobacco smoke causes skin ageing mediated by, for example, its effects on fibroblasts and keratinocytes (3)(4)(5), narrowing of blood vessels (6) and loss of vitamin C (7), no studies to date have directly evaluated the mechanisms underlying smoker's pigmentation. Skin pigmentation results from an increased production of melanins.…”

Section: Introductionmentioning

confidence: 99%

“…The SCF/c-kit pathway is also reported to mediate UVB-induced melanogenesis via the AhR (11). AhR bind several exogenous ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and is involved in skin ageing (5). TCDD-induced AhR also regulate skin pigmentation (12).…”

Section: Introductionmentioning

confidence: 99%

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Tobacco smoke–induced skin pigmentation is mediated by the aryl hydrocarbon receptor

Nakamura

Ueda

Hayashi

et al. 2013

Experimental Dermatology

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It is widely recognized that tobacco smoke causes skin pigmentation. No studies, however, have directly evaluated the mechanisms of the changes in smoker's skin pigmentation. In this study, when cultured with water-soluble tobacco smoke extract, the human epidermal melanocytes grew to a large size and produced more melanins. We evaluated melanocyte activation by quantifying microphthalmia-associated transcription factor (MITF) expression by real-time polymerase chain reaction. MITF expression was significantly and dose-dependently increased by exposure to tobacco smoke extract. The Wnt/b-catenin signalling pathway seemed to mediate the tobacco smoke extract-induced melanocyte activation. Immunocytochemical studies revealed that the activated melanocytes actively expressed aryl hydrocarbon receptors (AhR) around the nuclear membrane. The tobacco smoke extract-induced MITF activation was inhibited by RNA silencing of the AhR. This study provides the evidence that tobacco smoke enhances pigmentation in vitro and that the increase in pigmentation may involve b-catenin-and AhR-mediated mechanisms inside human melanocytes.

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Section: Accepted For Publication 17 June 2013mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Tobacco smoke–induced skin pigmentation is mediated by the aryl hydrocarbon receptor

Nakamura

Ueda

Hayashi

et al. 2013

Experimental Dermatology

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“…Tobacco smoke contains more than 3800 constituents, including numerous water-insoluble polycyclic aromatic hydrocarbons (PAHs) that trigger aryl hydrocarbon receptor (AhR) signalling pathways. To analyse the molecular mechanisms involved in tobacco smoke-induced skin aging [97].…”

Section: Effects Of Smokingmentioning

confidence: 99%

“…These findings suggest that the tobacco smoke extracts induce MMP-1 expression in human fibroblasts and keratinocytes via activation of the AhR pathway. Thus, the AhR pathway may be pathogenetically involved in extrinsic skin ageing [97].…”

Section: Effects Of Smokingmentioning

confidence: 99%

Review of Major Theories of Skin Aging

Gragnani

Cornick²,

Chominski³

et al. 2014

AAR

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Here we aim to describe each factor that leads to skin aging and describe their mechanisms. A PubMed database searches (from January 2004 to March 2014) using aging and skin as searched terms. There are substantial evidences showing that aging is associated with damage from free radicals represented by various reactive oxygen species (ROS). Mitochondria are producers and also targets of oxidative stress. The cycle of mitochondrial dysfunction can trigger the aging process. In the cellular senescence and telomeres theory, the diploid cells exhibit a limited proliferation potential. After a finite number of divisions, they enter a state of senescence with a stop replication in cell proliferation. It is suggested that aging is associated mainly with hyper-regulation of apoptosis. Obesity presumably accelerates the process of aging, which is aggravated by smoking. And the influence of the environment, called solar UV irradiation is of considerable importance to skin aging. There are several mechanisms that trigger the natural aging process and contribute to age-related changes, including oxidative stress theory of free radicals, the mitochondrial dysfunction, telomere shortening, UV radiation and other mechanisms that taken together or alone may or not accelerate the change in skin.

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Involvement of 4‐hydroxy‐2‐nonenal in pollution‐induced skin damage

et al. 2019

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The effects of environmental insults on human health are a major global concern. Some of the most noxious pollutants that humans are exposed to include ozone (O3), particulate matter (PM), and cigarette smoke (CS). Since the skin is the first line of defense against environmental insults, it is considered one of the main target organs for the harmful insults of air pollution. Thus, there is solid evidence that skin pathologies such as premature aging, atopic dermatitis (AD), and psoriasis are associated with pollutant exposure; all of these skin conditions are also associated with an altered redox status. Therefore, although the mechanisms of action and concentrations of O3, PM, and CS that we are exposed to differ, exposure to all of these pollutants is associated with the development of similar skin conditions due to the fact that all of these pollutants alter redox homeostasis, increasing reactive oxygen species production and oxidative stress. A main product of oxidative stress, induced by exposure to the aforementioned pollutants, is 4‐hydroxy‐2‐nonenal (HNE), which derives from the oxidation of ω‐6 polyunsaturated fatty acids. HNE is a highly reactive compound that can form adducts with cellular proteins and even DNA; it is also an efficient cell signaling molecule able to regulate mitogen‐activated protein kinase pathways and the activity of redox‐sensitive transcription factors such as Nrf2, AP1, and NFκB. Therefore, increased levels of HNE in the skin, in response to pollutants, likely accelerates skin aging and exacerbates existing skin inflammatory conditions; thus, targeting HNE formation could be an innovative cosmeceutical approach for topical applications.

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Role of the aryl hydrocarbon receptor in tobacco smoke extract–induced matrix metalloproteinase‐1 expression

Cited by 78 publications

References 30 publications

Tobacco smoke–induced skin pigmentation is mediated by the aryl hydrocarbon receptor

Tobacco smoke–induced skin pigmentation is mediated by the aryl hydrocarbon receptor

Review of Major Theories of Skin Aging

Involvement of 4‐hydroxy‐2‐nonenal in pollution‐induced skin damage

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