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Microarray analysis of B16 cells in pigmentation oscillator

ABSTRACT: Cellular homeostasis is an outcome of complex interacting processes with nonlinear feedbacks that span spatiotemporal scales. Skin tanning is one such dynamic response that maintains genome integrity of epidermal cells. While pathways underlying hyperpigmentation cascade are recognized, negative feedback regulatory loops that can dampen the activated melanogenesis process are not completely understood. By designing a pigmentation oscillator, in this study we delineate the role of interferon gamma (IFN-γ) signaling in skin pigmentation homeostasis. IFN-γ signaling reversibly controls maturation of the key organelle melanosome by concerted regulation of several pigmentation genes. We show that this temporal effect is mediated through interferon regulatory factor-1 (IRF-1) independent of the central regulator microphthalmia-associated transcription factor (MITF). Chronic expression of IFN-γ in mouse and human skin shows hypopigmentation phenotype, further providing a strong support to the under-appreciated function of IFN-γ in skin pigmentation. Our studies thus reveal the hitherto missing link between immune system and pigmentation, which may have implications in depigmentary and malignant cutaneous disorders.

ORGANISM(S): Mus musculus

PROVIDER: GSE54359 | GEO | 2014/02/03

SECONDARY ACCESSION(S): PRJNA236317

REPOSITORIES: GEO

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Microarray analysis of B16 cells in pigmentation oscillator

Project description:Cellular homeostasis is an outcome of complex interacting processes with nonlinear feedbacks that span spatiotemporal scales. Skin tanning is one such dynamic response that maintains genome integrity of epidermal cells. While pathways underlying hyperpigmentation cascade are recognized, negative feedback regulatory loops that can dampen the activated melanogenesis process are not completely understood. By designing a pigmentation oscillator, in this study we delineate the role of interferon gamma (IFN-γ) signaling in skin pigmentation homeostasis. IFN-γ signaling reversibly controls maturation of the key organelle melanosome by concerted regulation of several pigmentation genes. We show that this temporal effect is mediated through interferon regulatory factor-1 (IRF-1) independent of the central regulator microphthalmia-associated transcription factor (MITF). Chronic expression of IFN-γ in mouse and human skin shows hypopigmentation phenotype, further providing a strong support to the under-appreciated function of IFN-γ in skin pigmentation. Our studies thus reveal the hitherto missing link between immune system and pigmentation, which may have implications in depigmentary and malignant cutaneous disorders. there are 12 samples from two consecutive cycles of pigmentation oscillator, termed set 1 and set 2 analysis is performed wrt to day 0 of first cycle

2014-02-03 | E-GEOD-54359 | biostudies-arrayexpress

UV-protection timer controls a trade-off between skin protection systems

Project description:Tanning is a skin protection mechanism against UV radiation. Pigment production initiates hours after exposure, and the mechanism controlling this delay was unknown. Here we reveal a skin UV-protection timer, governed by damped oscillatory dynamics of the melanocyte master regulator, MITF, which after UV exposure, synchronizes regulatory programs, first cell survival and later pigmentation. Remarkably, the same amount of UV dosage resulted in higher pigmentation of human skin when given every-other day compared to daily exposure. Daily UV exposure appears to perturb MITF dynamics, thus re-ordering the survival and pigmentation programs. This demonstrates that the skin is more sensitive to frequency than quantity of UV exposure. Mathematical modeling identified a double negative regulatory loop involving HIF1a and microRNA-148a that regulates MITF dynamics. Our study suggests evolutionary leverage of the UV-protection timer, as it evolved to induce maximum protection with minimum damage for the reduction of skin cancer risk.

2018-10-26 | GSE114764 | GEO

A single intradermal injection of IFN-gamma induces a psoriasis-like state in both non-lesional psoriatic and healthy skin

Project description:Psoriasis is a chronic, debilitating, immune-mediated inflammatory skin disease. As IFN-gamma is involved in many cellular processes, including activation of T cells and dendritic cells (DCs), antigen processing and presentation, cell adhesion and trafficking, and cytokine and chemokine production, IFN-gamma-producing Th1 cells were proposed to be integral to the pathogenesis of psoriasis. Recently, IFN-gamma was shown to enhance IL-23 and IL-1 production by DCs and subsequently induce Th17 cells, important contributors to the inflammatory cascade in psoriasis lesions. To determine if IFN-gamma indeed induces the pathways leading to the development of psoriasis lesions, a single intradermal injection of IFN-gamma was administered to an area of clinically normal, non-lesional skin of psoriasis patients and biopsies were collected 24 hours later. Although there were no visible changes in the skin, IFN-gamma induced molecular and histological features characteristic of psoriasis lesions. IFN-gamma increased a number of differentially expressed genes in the skin, including many chemokines concomitant with an influx of T cells and inflammatory DCs. Furthermore, inflammatory DC products TNF, iNOS, IL-23, and TRAIL were present in IFN-gamma-treated skin. Thus, IFN-gamma, which is significantly elevated in non-lesional skin compared to healthy skin, appears to be a key pathogenic cytokine that can induce the inflammatory cascade in psoriasis. RNA was isolated from whole skin punch biopsies of either healthy or non-lesional psoraisis patients at baseline or 24 hours after placebo or IFN-g injection.

2011-11-30 | E-GEOD-32407 | biostudies-arrayexpress

Smart-seq analysis comparing melanocytes from Spry1flox/flox mice tail epidermis to the melanocytes derived from Spry1 epidermis specific knockout mice tail and back epidermis

Project description:The function and survival of melanocytes is regulated by an elaborate network of paracrine factors synthesized mainly by epidermal keratinocytes. Keratinocytes and melanocytes respond to UV exposure by eliciting a tanning response. However, how keratinocytes and melanocytes interact in the absence of UV exposure is unknown. Here, we demonstrate that after Spry1 knockout in epidermal keratinocytes, melanocyte stem cells (McSCs) in the hair follicle exit the stem cell niche without depleting the pool of these cells. We also found that McSCs migrate to the epidermis in a Scf/C-kit-dependent manner induced by a tanning-like response resulting from Spry1 loss in epidermal keratinocytes. Once there, these cells differentiate into functional melanocytes. These findings show the potential for developing therapies for skin pigmentation disorders by manipulating McSCs.

2024-02-21 | GSE252889 | GEO

A single intradermal injection of IFN-γ induces a psoriasis-like state in both non-lesional psoriatic and healthy skin

Project description:Psoriasis is a chronic, debilitating, immune-mediated inflammatory skin disease. As IFN-γ is involved in many cellular processes, including activation of T cells and dendritic cells (DCs), antigen processing and presentation, cell adhesion and trafficking, and cytokine and chemokine production, IFN-γ-producing Th1 cells were proposed to be integral to the pathogenesis of psoriasis. Recently, IFN-γ was shown to enhance IL-23 and IL-1 production by DCs and subsequently induce Th17 cells, important contributors to the inflammatory cascade in psoriasis lesions. To determine if IFN-γ indeed induces the pathways leading to the development of psoriasis lesions, a single intradermal injection of IFN-γ was administered to an area of clinically normal, non-lesional skin of psoriasis patients and biopsies were collected 24 hours later. Although there were no visible changes in the skin, IFN-γ induced molecular and histological features characteristic of psoriasis lesions. IFN-γ increased a number of differentially expressed genes in the skin, including many chemokines concomitant with an influx of T cells and inflammatory DCs. Furthermore, inflammatory DC products TNF, iNOS, IL-23, and TRAIL were present in IFN-γ-treated skin. Thus, IFN-γ, which is significantly elevated in non-lesional skin compared to healthy skin, appears to be a key pathogenic cytokine that can induce the inflammatory cascade in psoriasis.

2011-11-30 | GSE32407 | GEO

UV effects in mouse melanocytes

Project description:Ultraviolet (UV) radiation is a major melanoma risk factor, yet underlying mechanisms remain poorly understood. Here we introduce a mouse model permitting fluorescence-aided melanocyte imaging and isolation following in vivo UV irradiation. We use expression profiling to show that activated neonatal skin melanocytes isolated following a melanomagenic UVB dose bear a distinct, persistent interferon-response signature, including genes associated with immunoevasion. UVB-induced melanocyte activation, characterized by aberrant growth and migration, was abolished by antibody-mediated systemic blockade of interferon-gamma (IFN-gamma), but not type-I interferons. IFN-gamma was produced by macrophages recruited to neonatal skin by UVB-induced chemokine receptor Ccr2 ligands. Admixed recruited skin macrophages enhanced transplanted melanoma growth by inhibiting apoptosis; notably, IFN-gamma blockade abolished macrophage-associated melanoma growth and survival. IFN-gamma-producing macrophages were identified in 70% of human melanomas examined. Our data reveal an unanticipated role for IFN-gamma in promoting melanocytic cell survival/immunoevasion, and suggest IFN-gamma-R signaling represents a novel therapeutic melanoma target. Biologic replicates of UVA- and UVB-treated mouse melanocytes, as well as untreated mouse melanocytes and mouse keratinocytes, were used to define melanocyte expression signatures associated with UV treatment.

2011-01-01 | E-GEOD-25164 | biostudies-arrayexpress

Transcriptome analysis of feather follicles reveals candidate genes and pathways associated with pheomelanin pigmentation in chickens

Project description:In order to reveal the candidate genes related to yellow plumage in Chinese chicken, a hybrid population of Huiyang Bearded chicken and White Leghorn chicken, and transcriptome data were generated from the yellow and white feather follicle of F3 population in two periods (7 and 11weeks) respectively, using RNA-seq. 127 common different expressed genes were obtained(DEGs) between two periods, these DEGs were mainly enriched in the Gene Ontology classes ‘developmental pigmentation’, ‘melanin biosynthetic process’, ‘melanosome organization’, ‘melanosome membrane’ and ‘melanosome’all related to the pigmentation process. And involved genes were considered as pigment genes that play important roles in melanogenesis. The results reveal key functional genes and possible molecular mechanisms for the elucidation of yellow plumage formation in Chinese indigenous chickens.

2020-03-14 | GSE146956 | GEO

Fiorentino 2006-7 dermatomyositis, lupus, control skin

Project description:Background: Dermatomyositis (DM) is an autoimmune disease that mainly affects the skin, muscle, and lung. The pathogenesis of skin inflammation in DM is not well understood. Methodology and Findings: We analyzed genome-wide expression data in DM skin and compared them to those from healthy controls. We observed a robust upregulation of interferon (IFN)-inducible genes in DM skin, as well as several other gene modules pertaining to inflammation, complement activation, and epidermal activation and differentiation. The interferon (IFN)-inducible genes within the DM signature were present not only in DM and lupus, but also cutaneous herpes simplex-2 infection and to a lesser degree, psoriasis. This IFN signature was absent or weakly present in atopic dermatitis, allergic contact dermatitis, acne vulgaris, systemic sclerosis, and localized scleroderma/morphea. We observed that the IFN signature in DM skin appears to be more closely related to type I than type II IFN based on in vitro IFN stimulation expression signatures. However, quantitation of IFN mRNAs in DM skin shows that the majority of known type I IFNs, as well as IFN gamma, are overexpressed in DM skin. In addition, both IFN-beta and IFN-gamma (but not other type I IFN) transcript levels were highly correlated with the degree of the in vivo IFN transcriptional response in DM skin. disease_state_design

2012-01-12 | E-GEOD-32245 | biostudies-arrayexpress

UV effects in mouse melanocytes

2011-01-01 | GSE25164 | GEO

Transcription profiling of human epidermal keratinocytes treated with IFN-gamma reveals IFN-gamma suppressed the expression of over 100 genes responsible for cell cycle, DNA replication and RNA metabolism.

Project description:Cultured epidermal keratinocyte controls used for IFNg, TNFa and IL1 treatment. Interferon (IFN)-gamma, is a multifunctional, immunomodulatory cytokine with cell type-specific antiviral activities, particularly important in skin, where it is implicated in many diseases ranging from warts to psoriasis and cancer. Since epidermis is our first line of defence against many viruses, we investigated the molecular processes regulated by IFN-gamma in keratinocytes using DNA microarrays. We identified the IFN-gamma-regulated keratinocyte-specific genes in keratinocytes, IFN-gamma-induced tight junction proteins, presumably to deny viruses paracellular routes of infection. Furthermore, differing from published data, we find that IFN-gamma suppressed the expression of keratinocytes differentiation markers including desmosomal proteins, cornified envelope components and suprabasal cytokeratins. Inhibition of differentiation may interfere with the epidermal tropism of viruses that require differentiating cells for growth, for example, papillomaviruses. As in other cell types, IFN-gamma induced HLA, cell adhesion and proteasome proteins, facilitating leukocyte attraction and antigen-presentation by keratinocytes. IFN-gamma also induced chemokine/cytokines specific for mononuclear cells. IFN-gamma suppressed the expression of over 100 genes responsible for cell cycle, DNA replication and RNA metabolism, thereby shutting down many nuclear processes and denying viruses a healthy cell in which to replicate. Thus, uniquely in keratinocytes, IFN-gamma initiates a well-organized molecular programme boosting host antiviral defences, obstructing viral entry, suppressing cell proliferation and impeding differentiation.

2007-10-26 | E-GEOD-440 | biostudies-arrayexpress

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