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Special Issue "Molecular Mechanisms of Hypo- and Hyper-Pigmentations in Human Melanocytes"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 July 2020).

Special Issue Editor

Prof. Dr. Genji Imokawa
E-Mail
Guest Editor
Center for Bioscience Research & Education, Utsunomiya University, 350 Mine Utsunomiya, Tochigi 321-8505, Japan
Interests: melanogenesis; cell signaling; atopic dermatitis; sphingolipid metabolism
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Although anti-pigmenting products in the cosmetic field are becoming more and more popular, little is known about the precisely established molecular mechanisms of hypo- and hyper-pigmentations in human melanocytes or human skin, despite the many hypotheses for such molecular mechanisms that have been proposed in experimental systems using B-16 melanoma cells, animal hair follicular pigment cells and animal skin. Thus, a major aim for this Special Issue is to clarify the molecular mechanisms of hypo- and hyper-pigmentations in human melanocytes or human skin, including UVA or UVB melanosis/leudodermia/vitiligous skin/melasma/solar lentigo/atopic dirty skin.
This Special Issue on “Molecular Mechanisms of Hypo- and Hyper-Pigmentations in Human Melanocytes” aims to provide a summary of the emerging field with emphasis on novel developments and novel results with different types of skin hyper- or hypo-pigmentation. The Special Issue also calls for original research and reviews, including perspectives in the field of the current standing of molecular mechanisms of hypo- and hyper-pigmentations. Papers on molecular mechanisms of new pigmenting regulatory products, introduction of idea for new ani-pigmenting agents, and new techniques for measuring the pigmentatin process are welcome.

Prof. Dr. Genji Imokawa
Guest Editor

Manuscript Submission Information

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Keywords

  • UVA
  • UVB
  • Melanogenesis
  • Tyrosinase
  • MITF
  • Atopic dermatitis
  • Vitiligous skin
  • Epidermal pigmentation

Published Papers (2 papers)

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Research

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Article
Melanogenic Properties and Expression Profiles of Melanogenic Paracrine Molecules in Riehl’s Melanosis
Int. J. Mol. Sci. 2020, 21(5), 1695; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21051695 - 02 Mar 2020
Viewed by 1419
Abstract
Riehl’s melanosis is a hyperpigmentary disorder that occurs predominantly on the face and neck. To date, the pathogenesis of Riehl’s melanosis with regards to the melanogenic properties and paracrine melanogenic molecules has not well been studied. This study was aimed to provide a [...] Read more.
Riehl’s melanosis is a hyperpigmentary disorder that occurs predominantly on the face and neck. To date, the pathogenesis of Riehl’s melanosis with regards to the melanogenic properties and paracrine melanogenic molecules has not well been studied. This study was aimed to provide a novel perspective on the pathogenesis of Riehl’s melanosis by identifying the relevant paracrine melanogenic molecules in Riehl’s melanosis. Skin biopsies were performed on lesional and normal-appearing perilesional skin of 12 patients with Riehl’s melanosis and 12 age- and sex-matched healthy controls. Histopathological and immunohistochemical staining for paracrine melanogenic molecules was analyzed. The major histopathological findings of Riehl’s melanosis were basal hyperpigmentation, melanocyte proliferation, interface change, dermal pigmentary incontinence, vascular proliferation, and dermal inflammation. Dermal expression intensities of stem cell factor (SCF) and c-kit were increased in the lesional skin of Riehl’s melanosis. In addition, increased expression of epidermal and dermal ET-1 was also observed in the lesional skin of Riehl’s melanosis. Increased tissue expressions of SCF, c-kit, and ET-1 in Riehl’s melanosis support the role of these paracrine melanogenic molecules in the pathogenesis of Riehl’s melanosis. The findings from this study might present useful information on the pathogenetic mechanism of Riehl’s melanosis. Full article
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Review

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Review
Elucidation of Melanogenesis Cascade for Identifying Pathophysiology and Therapeutic Approach of Pigmentary Disorders and Melanoma
Int. J. Mol. Sci. 2020, 21(17), 6129; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21176129 - 25 Aug 2020
Cited by 7 | Viewed by 1478
Abstract
Melanogenesis is the biological and biochemical process of melanin and melanosome biosynthesis. Melanin is formed by enzymic reactions of tyrosinase family proteins that convert tyrosine to form brown-black eumelanin and yellow-red pheomelanin within melanosomal compartments in melanocytes, following the cascades of events interacting [...] Read more.
Melanogenesis is the biological and biochemical process of melanin and melanosome biosynthesis. Melanin is formed by enzymic reactions of tyrosinase family proteins that convert tyrosine to form brown-black eumelanin and yellow-red pheomelanin within melanosomal compartments in melanocytes, following the cascades of events interacting with a series of autocrine and paracrine signals. Fully melanized melanosomes are delivered to keratinocytes of the skin and hair. The symbiotic relation of a melanocyte and an associated pool of keratinocytes is called epidermal melanin unit (EMU). Microphthalmia-associated transcription factor (MITF) plays a vital role in melanocyte development and differentiation. MITF regulates expression of numerous pigmentation genes for promoting melanocyte differentiation, as well as fundamental genes for maintaining cell homeostasis. Diseases involving alterations of EMU show various forms of pigmentation phenotypes. This review introduces four major topics of melanogenesis cascade that include (1) melanocyte development and differentiation, (2) melanogenesis and intracellular trafficking for melanosome biosynthesis, (3) melanin pigmentation and pigment-type switching, and (4) development of a novel therapeutic approach for malignant melanoma by elucidation of melanogenesis cascade. Full article
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