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The role of keratinocyte DDX5 in IMQ-induced psoriatic mice

ABSTRACT: The role of keratinocyte DDX5 in IMQ-induced psoriatic mice

PROVIDER: PRJNA860590 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20330112_1.fastq.gz	Fastqsanger.gz
	SRR20330112_2.fastq.gz	Fastqsanger.gz
	SRR20330113_1.fastq.gz	Fastqsanger.gz
	SRR20330113_2.fastq.gz	Fastqsanger.gz
	SRR20330114_1.fastq.gz	Fastqsanger.gz

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The role of keratinocyte DDX5 in IMQ-induced psoriatic mice

Project description:To investigate whether DDX5 is involved in the development of psoriasis,we performed gene expression profiling analysis using data obtained from RNA-seq of ear skins from Ddx5f/f and K14Ddx5f/f psoriatic mice

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Keratinocyte DDX5 in response to IL-36γ

Project description:To compare how WT and DDX5-/- keratinocyte in response toIL-36γ, we performed gene expression profiling analysis using data obtained from RNA-seq of WT and DDX5-/- keratinocyte stimulated by IL-36γ

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Group IVE Cytosolic Phospholipase A2 Limits Psoriatic Inflammation by Mobilizing the Anti-inflammatory Lipid N-Acylethanolamine

Project description:Psoriasis is an inflammatory disorder characterized by keratinocyte hyper-proliferation and Th17-type immune responses. However, the roles of bioactive lipids and the regulation of their biosynthesis in this chronic skin disease are not fully understood. Herein, we show that group IVE cytosolic phospholipase A2 (cPLA2epsilon/PLA2G4E) plays a counterregulatory role against psoriatic inflammation by producing the non-canonical anti-inflammatory lipid N-acylethanolamine (NAE). Lipidomics analysis of mouse skin revealed that NAE species and their precursors (N-acyl-phosphatidylethanolamine and glycerophospho-N-acylethanolamine) were robustly increased in parallel with the ongoing process of imiquimod (IMQ)-induced psoriasis, accompanied by a marked upregulation of cPLA2epsilon in epidermal keratinocytes. Genetic deletion of cPLA2epsilon/Pla2g4e exacerbated IMQ-induced ear swelling and psoriatic marker expression, with a dramatic reduction of NAE-related lipids in IMQ-treated, and even normal, skin. Stimulation of cultured human keratinocytes with psoriatic cytokines concomitantly increased PLA2G4E expression and NAE production, and supplementation with NAEs significantly attenuated the cytokine-induced upregulation of the psoriatic marker S100A9. Increased expression of cPLA2epsilon was also evident in the epidermis of psoriatic patients. These findings reveal for the first time the in vivo role of cPLA2epsilon, which is highly induced in the keratinocytes of the psoriatic skin, promotes the biosynthesis of NAE-related lipids, and contributes to limiting psoriatic inflammation.

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The role of keratinocyte DDX5 in MC903-induced atopic dermatitis (AD) mice

Project description:The role of keratinocyte DDX5 in MC903-induced atopic dermatitis (AD) mice

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Keratinocyte DDX5 in response to IL-36γ

Project description:Keratinocyte DDX5 in response to IL-36γ

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Project description:The role of keratinocyte ferroptosis in IMQ-induced psoriatic mice

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Calcium/calmodulin-dependent protein kinase IV promotes imiquimod-induced psoriatic inflammation via macrophages and keratinocytes in mice

Project description:CaMK4 has an important function in autoimmune diseases, and the contribution of CaMK4 in psoriasis remains obscure. Here, we show that CaMK4 expression is significantly increased in psoriatic lesional skin from psoriasis patients compared to healthy human skin as well as inflamed skin from an imiquimod (IMQ)-induced mouse model of psoriasis compared to healthy mouse skin. Camk4-deficient (Camk4−/−) mice treated with IMQ exhibit reduced severity of psoriasis compared to wild-type (WT) mice. There are more macrophages and fewer IL-17A+γδ TCR+ cells in the skin of IMQ-treated Camk4−/− mice compared to IMQ-treated WT mice. CaMK4 inhibits IL-10 production by macrophages, thus allowing excessive psoriatic inflammation. Deletion of Camk4 in macrophages alleviates IMQ-induced psoriatic inflammation in mice. In keratinocytes, CaMK4 inhibits apoptosis as well as promotes cell proliferation and the expression of pro-inflammatory genes such as S100A8 and CAMP. Taken together, these data indicate that CaMK4 regulates IMQ-induced psoriasis by sustaining inflammation and provides a potential target for psoriasis treatment.

2022-05-28 | GSE204832 | GEO

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Project description:TREX2 is a keratinocyte specific 3â-deoxyribonuclease that participates in the maintenance of skin homeostasis upon damage. This transcriptome analysis identified multiple genes and pathways deregulated by TREX2 loss in the IMQ-induced psoriasis-like model in mouse skin. mRNA sequencing of 5 biological replicates of skin from wild-type mice treated with Imiquimod and 6 of Trex2 knockout mice treated with Imiquimod

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