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Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2

ABSTRACT: Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2

PROVIDER: PRJNA419494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6315890.fastq.gz	Fastqsanger.gz
	SRR6315891.fastq.gz	Fastqsanger.gz
	SRR6315892.fastq.gz	Fastqsanger.gz
	SRR6315893.fastq.gz	Fastqsanger.gz
	SRR6315894.fastq.gz	Fastqsanger.gz

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Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Epidermis ssRNA-Seq]

Project description:Arp2/3 complex assembles branched actin filaments key to many cellular processes, but its organismal roles remain poorly understood. Here we employed conditional arpc4 knockout mice to study the function of the Arp2/3 complex in the epidermis.We found that depletion of the Arp2/3 complex by knockout of arpc4 results in skin abnormalities at birth that evolve into a severe psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2. Knockout of arpc4 in cultured keratinocytes was sufficient to induce nuclear accumulation of Nrf2, upregulation of Nrf2-target genes and decreased filamentous actin levels. Furthermore, pharmacological inhibition of the Arp2/3 complex unmasked the role of branched actin filaments in Nrf2 regulation. Consistently, we unveiled that Nrf2 associates with the actin cytoskeleton in cells and binds to filamentous actin in vitro Finally, we discovered that Arpc4 is downregulated in both human and mouse psoriatic epidermis. Thus, the Arp2/3 complex affects keratinocytes' shape and transcriptome through an actin-based cell-autonomous mechanism that influences epidermal morphogenesis and homeostasis.

2017-11-23 | GSE107265 | GEO

Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Keratinocytes ssRNA-Seq]

2017-11-23 | GSE107264 | GEO

Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Epidermis ssRNA-Seq]

Project description:Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Epidermis ssRNA-Seq]

| PRJNA419518 | ENA

Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Keratinocytes ssRNA-Seq]

Project description:Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Keratinocytes ssRNA-Seq]

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Gene expression profile of epidermis from psoriasis lesions and healthy controls

Project description:Psoriasis is characterized by hyperplasia and disrupted differentiation of keratinocytes. Keratinocytes are considered not only the target but also the critical participants. To explore the role of keratinocytes in psoriasis, we used microarrays to compared gene expression profile of epidermis between psoriasis lesions and healthy normal skin.

2021-02-09 | GSE166388 | GEO

Single-cell transcriptomic analysis identifies infiltrating plasmacytoid dendritic cells in psoriasis epidermis

Project description:The study focuses on the cellular composition of the psoriasis epidermis, using single-cell transcriptomics to identify cell subsets and their interactions in both healthy and psoriatic skin. The research uncovers three keratinocyte populations and seven immune cell subsets exclusive to psoriatic lesions. A significant finding is the identification of a previously undetected population of plasmacytoid dendritic cells (pDCs) in the psoriatic epidermis, suggesting their role in the disease's pathogenesis. The study also highlights enhanced keratinocyte-immune cell interactions in psoriatic lesions, contributing to our understanding of psoriasis at the cellular level.

2024-06-25 | GSE254707 | GEO

Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-11-23 | GSE107266 | GEO

Gene expression profile of epidermis from psoriasis lesions and healthy controls

Project description:Gene expression profile of epidermis from psoriasis lesions and healthy controls

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T cell stimulation of resolved and non lesional epidermis- psoriasis patients

Project description:T cell stimulation of resolved and non lesional epidermis- psoriasis patients

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Spatial transcriptomics revealed that S1pr2 deletion in keratinocytes increases the MyD88/NF-kB pathway and psoriasis-related cytokine expression in the epidermis

Project description:The importance of the cross-talk between keratinocytes and immune cells in the pathogenesis of psoriasis has recently been reaffirmed. Recent studies have found that several S1PR functional antagonists, other than S1PR2, are effective in improving psoriasis. We performed spatial transcriptomics to map the immune cell landscape and its association with metabolic pathways in an imiquimod (IMQ)-induced psoriasis-like inflammation in S1pr2fl/fl K14-Cre mice that could not sense sphingosine-1-phosphate (S1P) in the epidermis through the S1PR2 receptor. Our analysis suggests that S1PR2 in keratinocytes plays a major role in psoriasis-like inflammation compared to other S1PRs. It acts as a down-regulator, inhibiting the recruitment of Th17 cells into the skin.

2024-09-20 | GSE277246 | GEO

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