Effect of MelasolvTM treatment on human melanocytes
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ABSTRACT:
PROVIDER: PRJNA955362 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the effect of MelasolvTM, we established human epidermal melanocytes cell lines in which MelasolvTM was treated for 1day. We then performed comparative gene expression profiling analysis using data obtained from RNA-seq of untreated and MelasolvTM-treated cells.
2023-10-02 | GSE229700 | GEO
Project description:Activating NRAS mutations in melanocyte precursor cells initiate congenital melanocytic nevi (CMN). Lesional cells reside in a state of oncogene-induced senescence. Here, we show that melanocytes undergoing NRAS-induced senescence exhibit profound alterations in lipid metabolism, together with elevated ferrous iron and lipid peroxidation. We further show that aldehyde dehydrogenase (ALDH) enzymes protect senescent melanocytes from ferroptosis by limiting lipid peroxidation and damage by lipid-derived aldehydes. Inhibition of ALDH1A1, ALDH1A3 and ALDH1B1 selectively eliminated senescent melanocytes by triggering ferroptotic lipid peroxidation and downstream aldehyde-mediated damage, an effect amplified by SLC7A11 inhibition. In a murine CMN model and in ex vivo cultured human CMN tissue, ALDH inhibition selectively depleted nevus cells. Melanoma cells induced into a senescence-like state by targeted therapy were similarly sensitized to ferroptosis upon ALDH inhibition. The dependence of senescent melanocytes and melanoma cells on ALDH enzymes to evade ferroptosis constitutes a selectively targetable therapeutic vulnerability.
2026-09-09 | GSE345642 | GEO
Project description:Transcriptomics of vitiligo melanocytes after hydroxychloroquine treatment
| PRJNA779610 | ENA
Project description:Melanocytes are surrounded by diverse cells including sensory neurons in our skin, but their interaction and functional importance has been poorly investigated. In this study, we found that melanocytes and nociceptive neurons contact more in human skin color patch tissue than control. Co-culture with human iPS cell-derived sensory neurons significantly induced morphogenesis and pigmentation of human melanocytes. To reveal melanocytes-stimulating factors secreted from neurons, we performed proteomic analyses and identified RGMB in the sensory neuron-conditioned media. RGMB protein induced morphogenesis and melanin production of melanocytes, demonstrating that RGMB is a melanocyte-stimulating factor released from sensory neurons. Transcriptome analysis suggested that the melanosome transport machinery could be controlled by RGMB, which led us to identify vesicle production response of melanocytes upon RGMB treatment. This study discovered a role of sensory neurons to modulate multiple aspects of human melanocytes through secretion of a key factor RGMB.
2022-08-08 | GSE189493 | GEO
Project description:Effect of inducible overexpression of NRASWT or NRASQ61R in human epidermal melanocytes
| PRJNA1521399 | ENA
Project description:Notch1 Activation Confers Transforming Properties to Primary Human Melanocytes and Promotes Human Melanoma Progression We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Human neonatal melanocytes and Notch transformed human neonatal melanocytes were selected for RNA extraction and hybridization on Illumina gene expression array chip. Expression intensities were calculated and normalized for each gene probed on the array for all hybridizations using illumina Beadstudio#3 software. Microarray analyses were subsequently performed in GeneSpring to aid in the identification of genes differentially-expressed between Notch-infected and control melanocytes that may be responsible for the phenotypic changes described in the NIC-infected cells.
2010-06-25 | E-GEOD-15040 | biostudies-arrayexpress
Project description:Vitiligo, an acquired disorder characterized by depigmented skin patches, results from loss of epidermal melanocytes. Etiology of vitiligo is not clearly understood but environmental, biochemical, genetic, and immune factors play a role in its pathogenesis. There is evidence that melanocyte death is perpetuated by an autoimmune response that causes lesions to spread. 4-tertiary butyl phenol (4TBP) and monobenzyl ether of hydroquinone (MBEH) are phenolic compounds that are known as environmental causes of vitiligo. We used microarray to detail the global gene expression that occurs following exposure of melanocytes to 4-TBP or MBEH to identified distinct classes of up-regulated genes that may contribute to melanocyte loss in vitiligo. We show that human melanocytes exposed to 4-TBP and MBEH show increased production of some inflammatory cytokines. Interleukin-6 (IL6) and IL8, in particular, are expressed at the periphery of vitiligo lesions and may contribute to recruitment of immune components to the areas, perpetuating melanocyte loss. Cultured human epidermal melanocytes were treated with 4TBP or MBEH for 3, 6, or 24 hours and gene expression were compared with untreated cells.
2012-12-01 | E-GEOD-31641 | biostudies-arrayexpress
Project description:Little is known about the mechanisms underlying the localization of human melanocytes during embryogenesis, and how the characteristics of melanocytes differ in various body sites. Immunohistochemical studies of biopsy tissue obtained from four different anatomic sites (scalp, back, abdomen, and sole) of 31 aborted fetuses following the approval of the ethics committee for the study of human gene analysis revealed that the melanocyte-associated marker gp100 was expressed earlier in embryogenesis than other melanocyte markers. Human fetal melanocytes are initially localized in the epidermis, and then migrate to the hair buds from the epidermis but not the dermis. In the sole, melanocytes localize in eccrine sweat gland ducts. Cultured fetal melanocytes did not stain positively for any melanocyte markers other than MITF and nestin. When co-cultured with normal human keratinocytes and fibroblasts, fetal melanocytes stained positively for gp100. Gene expression studies indicated that fetal melanocytes were topographically diverse, especially sole-derived melanocytes compared with other melanocytes. Expression of several genes, including CHI3L1 and FGF7, was higher in sole-derived melanocytes. These findings suggest that human fetal melanocytes derived from the sole have different profiles both in vivo and in vitro compared with melanocytes from other sites.
2011-05-01 | GSE24041 | GEO
Project description:Aims: This study aims to assess the effect of simultaneous use of cannabigerol (CBG) and 3-O-ethyl ascorbic acid (EAA) on changes in the skin melanocyte proteome induced by UVA radiation, with particular emphasis on modifications in the structure of metabolically important proteins. Results: Proteomic analysis allowed to identify 1248 proteins with statistically significantly changed expression following melanocytes irradiation and/or incubation with CBG/EAA. The top 25 proteins with most strongly modified expression included mainly proteins involved in cells protection/antioxidant response, as well as pro-inflammatory and proapoptotic signalization. Moreover, in melanocytes irradiated with UVA, the levels of lipid peroxidation product, 4-hydroxynonenal (4-HNE) and its protein adducts increase, as well as significant changes in the profile of proteins modified by 4-HNE are observed. CBG and EAA, especially when used together, largely reverse this effect. Innovation: This study for the first time shows the combined effect of CBG and EAA on the proteome of melanocytes after their exposure to UVA radiation, that applies to both changes in protein expression and intracellular signaling based on protein modification by lipid peroxidation products. Conclusion: It can be summarized that CBG and EAA can provide melanocytes with the most effective protection against oxidative stress, and perhaps even protect the skin structure against carcinogenesis.
2026-06-15 | PXD074276 | Pride
Project description:Effect of LIF treatment on human macrophages
| PRJNA872941 | ENA