China
Africa
Explore chapters and articles related to this topic
Dermal Hypersensitivity: Immunologic Principles and Current Methods of Assessment
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
A mutant strain of mouse, the C57Bl/Ler-vit/vit, exhibits a loss of epidermal pigment cells and a selective cell-mediated deficiency to epicutaneously administered allergens. This observation is consistent with humans with vitiligo, a disorder where pigment cells are destroyed and frequent autoimmunity occurs, along with a loss of contact hypersensitivity.197 Since other immune components were normal and contact hypersensitivity responses could be restored with skin transplants, this vit/vit strain of mouse could serve in an excellent role for the investigation of various aspects of contact hypersensitivity reactions.
Repigmentation in Vitiligo
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Bharat Bhushan Mahajan, Richa Nagpal
During in vitro stimulation of pigment cells, several cytokines have been observed to have different effects: PGD2, LTB4, LTC4, LTD4, LTE4, thromboxane B2, and HETE produce increased dendricity, edema, higher levels of tyrosinase, and immunoreactive b-locus [22,23];Other cytokines including transforming growth factor alpha, basic fibroblast growth factor (bFGF), stem cell factor (SCF) and endothelin-1 (ET-1), increase melanocyte migration [24,25]; some of these cytokines (LTB4, LTC4, ET-1, EGF) are involved in both functions.
A Transcriptomic Analysis and shRNA Screen for Intracellular Ion Channels and Transporters Regulating Pigmentation
Published in Bruno Gasnier, Michael X. Zhu, Ion and Molecule Transport in Lysosomes, 2020
Donald C. Koroma, Salwa Y. Hafez, Elena Oancea
Rationale: Melanosomes are organelles unique to pigment cells, including epidermal melanocytes. We reasoned that proteins critical for the ability of melanosomes to produce melanin can be encoded by either (i) genes that are unique to pigment cells, similar to those mutated in different types of OCA, or (ii) genes that serve different roles in other cells and in melanocytes are localized to and repurposed to function in melanosomes, similar to TPC2, a lysosomal channel in other cells. Because melanocytes contain a large number of melanosomes, melanosomal proteins will presumably be expressed at high levels in melanocytes, but not in other cells.
Development of piperine nanoemulsions: an alternative topical application for hypopigmentation
Published in Drug Development and Industrial Pharmacy, 2022
Burcu Ozkan, Ebru Altuntas, Rabia Cakir Koc, Yasemin Budama-Kilinc
Melanin biosynthesis is a complex mechanism that occurs within melanocytes, very specialized pigment cells within membrane-bound organelles called melanosomes [1]. Melanogenesis has different stages, and when this process is disrupted, different types of pigmentation disorders can be seen, classified as hypo- or hyperpigmentation [2,3]. Melanocytes are largely destroyed in hypopigmentation disorders such as vitiligo due to the loss of functional epidermal melanocytes. Therefore, depigmented lesions occur on the skin [4]. Vitiligo is a common disease affecting 0.5–2% of the general population. This bothersome disease begins on average at the age of 20 but is most common between the ages of 10 and 30 [5]. This apparent disorder can lead to many psychological, social and physiological problems in individuals [6].
Value of silicone gel in prevention of cobblestoning following punch minigrafting in vitiligo
Published in Journal of Dermatological Treatment, 2022
Tag Anbar, Talal Abd El Raheem, Dalia Ahmed Bassiouny, Marwa Mohamed Fawzy, Zeinab El Maadawi, Noha Farouk, Mohamed Hassan
In a trial to understand the immunohistochemical background of cobblestoning phenomenon after punch grafting of vitiligenous skin, two markers which were thought to have a role in both melanoblast migration and wound healing process were chosen. Matrix metalloproteinase 9 (MMP) is of the MMP family. It is responsible for degradation and remodeling of extracellular matrix (ECM). For repigmentation, timely degradation of ECM is an important feature of melanoblast migration (8). MMPs play central roles in morphogenesis, wound healing, tissue repair, migration and remodeling in response to an injury (9,10). Tenascin-C inhibits adhesion of melanocytes to fibronectin and this anti-adhesive effect may contribute to the loss of pigment cells in vitiligo. It is also expressed de novo during wound healing or in pathological conditions, including chronic inflammation (11,12).
GPR143 genotypic and ocular phenotypic characterisation in a Chinese cohort with ocular albinism
Published in Ophthalmic Genetics, 2021
Junwei Zhong, Bing You, Ke Xu, Xiaohui Zhang, Yue Xie, Yang Li
OA1 is caused by mutations in the G protein-coupled receptor 143 (GPR143) gene in Xp22.2; this gene covers about 40 kb of genomic DNA and has nine coding exons. It encodes a 404 amino acid protein (5,6), the GPR143 protein. This protein is a G protein-coupled receptor (GPCR) that is exclusively expressed in the retinal pigment epithelium (RPE) and melanocytes (7). Unlike all other GPCRs, which are distributed in plasma membranes, GPR143 is situated in melanosomes in the pigment cells and in lysosomes in non-pigment cells (8). The GPR143 function might involve regulation of melanosome transport in pigment cells, and it plays an important role in melanosome biogenesis (8). At present, over 60 mutations of the GPR143 gene have been described, with most being nonsense, splicing effect, frameshift small insert or deletions, or large deletions involving partial or complete GPR143 genes. These mutation types imply that OA1 is caused by a loss-of-function mechanism (2,5,6,9–15).