Hiramoto K, Kobayashi H, Ishii M et al.Increased alpha-melanocyte-stimulating hormone (α-MSH) levels and melanocortin receptors expression associated with pigmentation in an NC/Nga mouse model of atopic dermatitis. Exp Dermatol 19:132-136

Department of Biochemistry and Molecular Pathology, Osaka City University Medical School, Osaka, Japan.
Experimental Dermatology (Impact Factor: 3.76). 11/2009; 19(2):132-6. DOI: 10.1111/j.1600-0625.2009.00988.x
Source: PubMed


Please cite this paper as: Increased alpha-melanocyte-stimulating hormone (α-MSH) levels and melanocortin receptors expression associated with pigmentation in an NC/Nga mouse model of atopic dermatitis. Experimental Dermatology 2010; 19: 132–136.
Abstract: Patients with a specific subtype of atopic dermatitis (AD) display particular patterns of pigmentation, such as ripple pattern pigmentation on the neck, pigmented macules on the lip and diffuse pigmentation. However, the mechanism underlying these patterns has not been determined. The purpose of our research is to investigate the factors influencing this type of pigmentation in AD. We observed that AD model mice (NC/Nga mice) displayed an increase in the number of 3, 4-dihydroxyphenylalanine (Dopa)-positive melanocytes in the epidermis and intestine (jejunum and colon) while in the inflammatory state. The plasma levels of alpha-melanocyte-stimulating hormone (α-MSH) and adrenocoticotropin (ACTH) also increased in NC/Nga mice with dermatitis. Furthermore, the expression of melanocortin receptor 5 and melanocortin receptor 1 (MC1R) increased in the skin, and melanocortin receptor 3 (MC3R) expression increased in the intestine. However, the changes in the Dopa-positive cells of conventional NC/Nga mice were not induced by treatment with either agouti (an MC1R antagonist) or agouti-related protein (an MC3R antagonist). These results indicate that the pigmentation of AD is related to increased levels of α-MSH, MC1R (in the skin) and MC3R (in the intestines).

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    • "Keratinocytes produce chemokines and these factors are involved with the development of inflammatory skin diseases, such as atopic dermatitis [23]. Chemokines can lead to a Th1/Th2 imbalance, which results in the development of atopic dermatitis lesions [4]. "
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    ABSTRACT: To elucidate the possible involvement of nitric oxide (NO) derived from inducible NO synthase (iNOS) in the pathogenesis of patients with allergic rhinitis, we used an animal model of atopic dermatitis (AD) induced by epicutaneous sensitization and analysed the differences in ear thickness, the frequency of scratching and plasma levels of ovalbumin-specific immunoglobulin E (OVA-IgE), transforming growth factor (TGF)-β, tumor necrosis factor (TNF)-α, adrenocorticotropic hormone (ACTH) and α-melanocyte-stimulating hormone (α-MSH) between control and iNOS(-/-) mice. Eight-week-old control and iNOS(-/-) male C57BL/6j mice were sensitized three times with OVA antigen. Before and after the last skin sensitization, the number of scratching incidents and the thickness of the ear were examined, and the plasma levels of OVA-IgE, α-MSH, ACTH, TGF-β and TNF-α were analysed by ELISA. Sensitization of mice with OVA resulted in increased plasma levels of OVA-IgE, α-MSH, ACTH, TGF-β and TNF-α in control, but not in iNOS(-/-) mice. The administration of l-nitro-arginine-methyl ester (l-NAME) abolished all the above changes that occurred in the control mice. In addition, iNOS(-/-) mice given α-MSH exhibited a change similar to that seen in the control, whereas iNOS(-/-) mice given ACTH, TGF-β or TNF-α did not demonstrate any changes. These results indicate that symptoms of AD such as scratching can be exacerbated by α-MSH, which is induced by iNOS-derived NO.
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    ABSTRACT: Abbreviations: α-MSH, α-melanocyte-stimulating hormone; AD, atopic dermatitis; GPCR, G protein–coupled receptors; MC-R, melanocortin receptor; NDP-α-MSH, [Nle4, D-Phe7]-α-MSH; TNP-IgE Tg mice, 2,4,6-trinitrophenol-specific IgE transgenic mice; TNP11-OVA, TNP-conjugated ovalbumin
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