Atopic Dermatitis: a Short Summary
- Smoking tobacco is known for inducing skin pigmentation.
- In vitro the authors cultures human epidermal melanocytes.
- When cultured with tobacco smoke extract:
- Pigment cells (melanocytes) grew to a large size and produced more melanin.
- Some melanocytes were irradiated with UVB light (another cause of pigmentation), and a similar production of melanin was observed. However the morphology of melanocytes was unaltered.
- Melanocyte activity can be estimated by measuring Microphthalmia-associated transcription factor (MITF) expressions by real-time PCR (Polymerase Chain Reaction).
- MITF expressions were significantly and dose-dependently increased by tobacco smoke extract (simlarly to increased doses of UVB).
- The Wnt/β-catenin signaling pathway seemed to mediate these melanocyte activations by tobacco smoke, because β-catenin expressions were increased only by tobacco smoke not by UVB irradiations.
- On the other hand, hese results indicate that UVB-induced melaninogenesis might be mediated by another pathway, for example the α-MSH or the SCF/c-kit pathway.
- Immunocytochemical studies revealed that tobacco activated melanocytes actively-expressed the aryl hydrocarbon receptors (AHR) around the nuclear membrane. This tobacco smoke-induced MITF activation was inhibited by RNA silencing of the aryl hydrocarbon receptors.
- Comment:
- Pigmentation by tobacco is probably done through activation of the the Wnt/β-catenin signaling pathway following stimulation of the AHR receptor (dioxin receptor).
Contributors:
Dr Christophe HSU – dermatologist. Geneva, Switzerland
Source de Information: M Nakamura, Y Ueda, T Furuhashi and A Morita Department of Geriatric and Environmental Dermatology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan. Tobacco smoke-induced skin pigmentation is mediated by the Wnt/β-catenin pathway and the aryl hydrocarbon receptor signaling. International Investigative Dermatology (IID) 2013 – Edinburgh, United Kingdom
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