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Gene expression profile of primary epidermal keratinocytes (HEKs) stimulated with lawsone

ABSTRACT: The study aimed to interrogate whether the 1,4-naphtoquinone derivative lawsone activates the aryl hydrocarbon receptor (AhR) downstream transcriptional program in keratinocytes and is capable of modulating skin homeostasis. The study has been performed on human primary epidermal keratinocytes (HEKs), which represent the first line of defense against exogenous molecules. HEK cells were treated with the vehicle control DMSO (control), stimulated with lawsone or with the TLR2 ligand Pam2CSK4. Transcriptional profiles of HEK cells were studied to investigate the regulation of AhR -related genes, Nrf2-related genes and epidermal differentiation and keratin genes. We demonstrated that lawsone was sensed by keratinocytes and activated AhR. In particular, lawsone efficiently activated the transcriptional program of AhR and promoted keratinocyte differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE99901 | GEO | 2019/08/06

REPOSITORIES: GEO

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Project description:Human epidermal keratinocytes-neonatal(HEKs )sequencing

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Homo sapiens

Project description:Gene expression profile of primary epidermal keratinocytes (HEKs) stimulated with lawsone

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AHR-TFAP2A regulates epidermal differentiation in response to environmental cues [ChIP-seq]

Project description:The Aryl Hydrocarbon Receptor (AHR) is an environmental sensor and an indispensable regulator of epithelial homeostasis. To investigate AHR-mediated gene regulation, we performed a comprehensive transcriptomic and epigenomic analysis using human primary epidermal keratinocytes. Our results showed that AHR activation led to the induction of canonical transcription factors involved in epidermal differentiation as an early response, i.e. Transcription Factor AP-2α (TFAP2A), while epidermal differentiation-related genes, such as filaggrin and keratins, were activated as late responsive genes. The identified AHR-TFAP2A axis and its role in keratinocyte terminal differentiation was confirmed through AHR and TFAP2A knockout using CRISPR/Cas9. Our findings demonstrate that AHR regulates epidermal differentiation through the transient activation of specific transcription factors, such as TFAP2A, in response to environmental cues. The herein identified AHR-TFAP2A axis provides a promising target for the treatment of diseases related to skin barrier dysfunction.

2023-09-08 | GSE226046 | GEO

AHR-TFAP2A regulates epidermal differentiation in response to environmental cues [RNA-seq]

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AhR interactome in early embryonic development

Project description:The transcriptional program of early embryonic development is tightly regulated by a set of well-defined transcription factors that suppress premature expression of differentiation genes and sustain the pluripotent identity. It is generally accepted that this program can be perturbed by environmental factors such as chemical pollutants, however the precise molecular mechanisms remain unknown. The Aryl Hydrocarbon Receptor (AHR) is a widely expressed nuclear receptor that senses environmental stimuli and modulates target gene expression. Here, we show that ectopic activation of AHR during early differentiation disrupts the differentiation program via the chromatin remodeling complex NuRD. The activated AHR/NuRD complex altered the expression of differentiation-specific genes that control the first two developmental decisions without affecting the pluripotency program. These findings identify a novel mechanism that allows environmental stimuli to disrupt embryonic development through AHR signaling.

2018-02-26 | PXD006089 | Pride

Genome-wide binding profile of the AhR transcription factor in keratinocytes

Project description:Atopic dermatitis is increasing worldwide, correlating with air pollutions. Various organic components of pollutants activate transcription factor AhR (aryl-hydrocarbon receptor). We have established AhR-CA mice, whose keratinocytes express constitutive-active AhR, and these mice developed atopic dermatitis-like frequent scratching and allergic inflammation. In this study we performed ChIP-seq analyses and identified keratinocyte-specific AhR target genes, including inflammatory cytokines Tslp and IL33, and neurotrophic factor Artemin. While AhR-CA mice exhibited epidermal hyperinnervation and alloknesis leading to hypersensitivity to pruritus, blockade of Artemin alleviated these phenotypes. AhR-CA mice showed scratching-induced barrier insufficiency and enhanced sensitization to epicutaneously-applied antigens, recapitulating human atopic dermatitis. Consistently, AhR activation and Artemin expression was detected in the epidermis of atopic dermatitis patients and keratinocytes exposed to air pollutants. Thus, AhR in keratinocytes senses the environmental stimuli and responds to them through moderating inflammation. We propose a mechanism in which air pollution induces atopic dermatitis through AhR activation.

2016-11-13 | GSE72455 | GEO

AhR links air pollution and atopic dermatitis via Artemin induction

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Effects of hydroquinone on whole-genome scale transcription of human epidermal keratinocytes.

Project description:Hydroquinone (HQ) is a well-known phenolic compound that causes chemical leukoderma. Hydroquinone was once used as photographic developers for films and papers, and it is widely used as a topical application in skin whitening to reduce the color of skin. Recently, the United States Food and Drug Administration (US FDA) banned all over-the-counter products with hydroquinone due to its potential toxicity. Topical cream with hydroquinone up to 4% should be prescribed and used with specific caution. In this study, to elucidate the toxicological role of keratinocyte in the pathogenesis of chemical leukoderma, we analyzed genome-wide transcriptional data of cultured human epidermal keratinocytes (HEKs) treated with sub-cytotoxic hydroquinone concentration.

2019-07-21 | GSE126721 | GEO

Mus musculus

Project description:Transcriptional activation of AhR pathway in keratinocytes

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Temporal Transcriptomic Analysis of Human Primary Keratinocytes Exposed to β-naphthoflavone Highlights the Protective Efficacy of Skin to Environmental Pollutants

Project description:The skin covers almost the entire body and plays an important role in detoxification and elimination of xenobiotics. These processes are initiated following the binding of xenobiotics to the aryl hydrocarbon receptor (AhR), which leads to the expression of several detoxification enzymes. To gain some insights on their impacts on skin cells over time, a temporal transcriptional analysis using gene expression arrays was performed in human primary epidermal keratinocyte (HEK) cells exposed for 6, 24 and 48h to β-naphthoflavone (βNF), a potent agonist of AhR. Our results demonstrated that expression of genes related to xenobiotic, inflammation, and extracellular matrix remodeling was increased upon βNF treatment from 6h onwards. In contrast, the anti-oxidative response was seen mainly starting at 24h. While some of the genes controlled by the epidermal differentiation complex was induced as soon as 6h, expression of most of the S100 related genes located within the same chromosomal locus and keratin genes was increased at later times (24 and 48h). Altogether our transcriptomic data highlight that following βNF exposure, HEK cells elicited a protective xenobiotic response together with the activation of inflammation and keratinocyte regeneration. Later on these processes were followed by the stimulation of anti-oxidant activity and terminal differentiation.

2020-03-31 | GSE143748 | GEO

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