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The neuronal transcription factor NeuroD and its impact on the regulation of dendricity and pigmentation of melanocytes in postinflammatory hyperpigmentation of human skin

ABSTRACT: In order to test the gene expression profile in postinflammatory hyperpigmentation, micoarray studies were performed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE56803 | GEO | 2015/04/11

SECONDARY ACCESSION(S): PRJNA244676

REPOSITORIES: GEO

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The neuronal transcription factor NeuroD and its impact on the regulation of dendricity and pigmentation of melanocytes in postinflammatory hyperpigmentation of human skin

Project description:In order to test the gene expression profile in postinflammatory hyperpigmentation, micoarray studies were performed. Totally 14 subjects ( 7 at each phase) were treated by suction blister, and samples from treated area and corresponding control area ( from the same subjects) were taken at 1 week(t1), 2 weeks(t2), 4 weeks(t3), 6 weeks(t4), and 16 weeks(t5) after treatment. Paired samples from subject 6382 at 6th week were missing for microarray hybridization. Therefore, there are 138 array chips available for statistical analysis.

2015-04-11 | E-GEOD-56803 | biostudies-arrayexpress

Fibroblast-directed melanocyte recruitment via Cxcl12-Cxcr4 cascade promotes post-inflammatory hyperpigmentation and skin barrier protection in zebrafish

Project description:Post-inflammatory hyperpigmentation (PIH), a prevalent dermatological condition, is classically attributed to melanocyte overactivation in situ. However, the precise triggers and physiological significance of melanocyte responses remain elusive. Using an acetic acid corrosion-induced zebrafish PIH model, here we demonstrate that melanocyte migration to the inflammatory site is a key pathogenic driver of hyperpigmentation. This migration is largely orchestrated by fibroblasts, but not macrophages or neutrophils, which secrete the chemokine cxcl12a upon injury, recruiting melanocytes via the cxcl12a-cxcr4a signaling axis. Beyond hyperpigmentation, we reveal that melanocytes function as a dual protective barrier against both UV-induced DNA damage and microbial invasion in response to acetic acid corrosion-induced injury. Our findings provide new insights into PIH pathogenesis and uncover the non-canonical barrier functions of melanocytes in skin inflammation and repair.

2025-10-01 | GSE302529 | GEO

Skin hyperpigmentation index: a new practical method for unbiased automated quantification of skin hyperpigmentation.

Project description: Not available

| S-EPMC7496784 | biostudies-literature

SASH1 S519N variant links skin hyperpigmentation and premature hair graying to dysfunction of melanocyte lineage

Project description:A better understanding of human melanocyte and melanocyte stem cell (McSC) biology is essential for treating melanocyte-related diseases. This study employed an inherited pigmentation disorder carrying the SASH1S519N variant in a Hispanic family to investigate the SASH1 function in melanocyte lineage and the underlying mechanism for this disorder. We used a multidisciplinary approach, including clinical exams, human cell assays, yeast two-hybrid screening, and biochemical techniques. Results linked early hair graying to the SASH1S519N variant, a previously unrecognized clinical phenotype in hyperpigmentation disorders. We identified SASH1 as a novel regulator in McSC maintenance and discovered that TNKS2 is crucial for SASH1’s role in vitro. Additionally, the S519N variant is located in one of multiple tankyrase binding motifs and alters the binding kinetics and affinity of the interaction. In summary, this disorder showcases accelerated aging in human McSC, linking both gain and loss of pigmentation to McSC dysfunction in the same individuals. The findings offer new insights into the roles of SASH1 and TNKS2 in McSC maintenance and the molecular mechanisms of pigmentation disorders. We propose that a comprehensive clinical evaluation of patients with skin disorders should include an assessment and history of hair pigmentation loss.

2024-06-17 | GSE266293 | GEO

Stem Cell Factor-Inducible MITF-M Expression in Therapeutics for Acquired Skin Hyperpigmentation.

Project description:Rationale: Microphthalmia-associated transcription factor M (MITF-M) plays important roles in the pigment production, differentiation and survival of melanocytes. Stem cell factor (SCF) and its receptor KIT stimulate MITF-M activity via phosphorylation at the post-translation level. However, the phosphorylation shortens half-life of MITF-M protein over the course of minutes. Here, we investigated novel hypotheses of (i) whether SCF/KIT can regulate MITF-M activity through gene expression as the alternative process, and (ii) whether chemical inhibition of KIT activity can mitigate the acquired pigmentation in skin by targeting the expression of MITF-M. Methods: We employed melanocyte cultures in vitro and pigmented skin samples in vivo, and applied immunoblotting, RT-PCR, siRNA-based gene knockdown and confocal microscopy. Results: The protein and mRNA levels of MITF-M in epidermal melanocytes and the promoter activity of MITF-M in B16-F0 melanoma cells demonstrated that SCF/KIT could trigger the expression of MITF-M de novo, following the phosphorylation-dependent proteolysis of pre-existing MITF-M protein. SCF/KIT regulated the transcription abilities of cAMP-responsive element-binding protein (CREB), CREB-regulated co-activator 1 (CRTC1) and SRY-related HMG-box 10 (SOX10) but not β-catenin at the MITF-M promoter. Meanwhile, chemical inhibition of KIT activity abolished SCF-induced melanin production in epidermal melanocyte cultures, as well as protected the skin from UV-B-induced hyperpigmentation in HRM2 mice or brownish guinea pigs, in which it down-regulated the expression of MITF-M de novo at the promoter level. Conclusion: We propose the targeting of SCF/KIT-inducible MITF-M expression as a strategy in the therapeutics for acquired pigmentary disorders.

| S-EPMC6929618 | biostudies-literature

Loss-of-function mutations in the melanocortin-2-receptor (mc2r) lead to skin hyperpigmentation in teleost fish

Project description:Melanocortins regulate pigmentation via melanocortin receptors (MCRs), which exhibit high conservation across zebrafish and humans. MC2R is distinctive among melanocortin receptors in that it is activated exclusively by ACTH and requires Mrap1 for optimal functionality, in contrast to other receptors that possess the capacity to bind diverse ligands. Although the melanocortin 1 receptor (MC1R) is well characterised for its role in pigmentation, the function of MC2R remains largely unknown. This study examines the influence of MC2R on pigmentation by generating MC2R knockout zebrafish using the CRISPR/Cas9 system. The results demonstrated that the mc2rKO mutants exhibited pronounced hyperpigmentation, characterised by an elevated number of melanophores and xanthophores, while preserving the distinctive striped pattern and dorsoventral countershading. Gene expression analyses show an increase in the expression of genes involved in melanosome synthesis and melanin production, contributing to a darker phenotype, as well as genes associated with lipid metabolism and carotenoid accumulation, which result in enhanced yellow coloration. These results suggest that mc2r plays a role in modulating the development, distribution and metabolic activity of pigment cells.

2025-09-02 | GSE292242 | GEO

Ablation of casein kinase 1α in keratinocytes induces p53-dependent hyperpigmentation of the skin

Project description:Ablation of casein kinase 1α in keratinocytes induces p53-dependent hyperpigmentation of the skin

| PRJEB19436 | ENA

Melanocytes and pigmentation are affected in dopachrome tautomerase knockout mice.

Project description:The tyrosinase family comprises three members, tyrosinase (Tyr), tyrosinase-related protein 1 (Tyrp1), and dopachrome tautomerase (Dct). Null mutations and deletions at the Tyr and Tyrp1 loci are known and phenotypically affect coat color due to the absence of enzyme or intracellular mislocalization. At the Dct locus, three mutations are known that lead to pigmentation phenotype. However, these mutations are not null mutations, and we therefore set out to generate a null allele at the Dct gene locus by removing exon 1 of the mouse Dct gene. Mice deficient in Dct [Dct(tm1(Cre)Bee)] lack Dct mRNA and dopachrome tautomerase protein. They are viable and do not show any abnormalities in Dct-expressing sites such as skin, retinal pigment epithelium, or brain. However, the mice show a diluted coat color phenotype, which is due to reduced melanin content in hair. Primary melanocytes from Dct knockout mice are viable in culture and show a normal distribution of tyrosinase and tyrosinase-related protein 1. In comparison to the knockout, the slaty mutation (Dct(slt)/Dct(slt)) has less melanin and affects growth of primary melanocytes severely. In summary, we have generated a knockout of the Dct gene in mice with effects restricted to pigment production and coat color.

| S-EPMC381679 | biostudies-literature

SASH1 S519N variant links skin hyperpigmentation and premature hair graying to dysfunction of melanocyte lineage

Project description:SASH1 S519N variant links skin hyperpigmentation and premature hair graying to dysfunction of melanocyte lineage

| PRJNA1106514 | ENA

Thioredoxin Reductase 1 Modulates Pigmentation and Photobiology of Murine Melanocytes in vivo.

Project description:Pigment-producing melanocytes overcome frequent oxidative stress in their physiological role of protecting the skin against the deleterious effects of solar UV irradiation. This is accomplished by the activity of several endogenous antioxidant systems, including the thioredoxin antioxidant system, in which thioredoxin reductase 1 (TR1) plays an important part. To determine whether TR1 contributes to the redox regulation of melanocyte homeostasis, we have generated a selective melanocytic Txnrd1-knockout mouse model (Txnrd1mel‒/‒), which exhibits a depigmentation phenotype consisting of variable amelanotic ventral spotting and reduced pigmentation on the extremities (tail tip, ears, and paws). The antioxidant role of TR1 was further probed in the presence of acute neonatal UVB irradiation, which stimulates melanocyte activation and introduces a spike in oxidative stress in the skin microenvironment. Interestingly, we observed a significant reduction in overall melanocyte count and proliferation in the absence of TR1. Furthermore, melanocytes exhibited an elevated level of UV-induced DNA damage in the form of 8-oxo-2'-deoxyguanosine after acute UVB treatment. We also saw an engagement of compensatory antioxidant mechanisms through increased nuclear localization of transcription factor NRF2. Altogether, these data indicate that melanocytic TR1 positively regulates melanocyte homeostasis and pigmentation during development and protects against UVB-induced DNA damage and oxidative stress.

| S-EPMC10771865 | biostudies-literature

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