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

PROVIDER: PRJNA1105717 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28825774_1.fastq.gz	Fastqsanger.gz
	SRR28825774_2.fastq.gz	Fastqsanger.gz
	SRR28825775_1.fastq.gz	Fastqsanger.gz
	SRR28825775_2.fastq.gz	Fastqsanger.gz
	SRR28825776_1.fastq.gz	Fastqsanger.gz

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The role of keratinocyte DDX5 in IMQ-induced psoriatic mice

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

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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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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.

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Project description:Psoriasis is a complex chronic inflammatory skin disease, but the exact mechanism underlying its development remains elusive. We found the expression of SHP2 was significantly higher in skin lesions and human peripheral blood mononuclear cells derived from psoriatic patients than those from normal controls. determine whether SHP2 activity affects psoriasis pathogenesis, we treated the murine psoriatic model with SHP099, a potent allosteric inhibitor of SHP2. SHP099 ameliorates the IMQ-induced psoriatic development in mice with unclear molecular mechanism. To address that, single-cell RNA sequencing was performed to explore the role of SHP2 in all cell types in IMQ-induced mouse skin upon SHP099 treatment.

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Project description:Crosstalk between keratin-forming cells and aberrant immune cells due to immune imbalance is a key factor in the pathogenesis of psoriasis. Most of the current clinical treatments provide rapid symptomatic relief but bring side effects that should not be ignored. Tetrastigma hemsleyanum polysaccharides (THP) have significant immunomodulatory and anti-inflammatory properties. In this study, we used imiquimod (IMQ)-induced psoriasis mouse model and LPS/IL-6-stimulated HaCaT cell model. The potential and mechanism of action of THP for psoriasis treatment were assessed by Psoriasis Area Severity Index (PASI) score, histopathology, flow cytometry, Western blot, and reverse transcription-polymerase chain reaction. The signs and symptoms of psoriatic mice induced by IMQ were significantly relieved by percutaneous administration of THP, including the improvement of psoriatic skin signs (erythema, folds, scales), pathological changes, decreased PASI score, and decreased spleen index. Results of in vivo and in vitro studies suggest that THP inhibits abnormal cell proliferation and excessive inflammation at skin lesions, balances Th17 immune cells, and blocks the keratinocyte-Th17 cell cycle, thus playing a role in psoriasis treatment by a mechanism that may be related to the regulation of the JAK/STAT3 signaling pathway.

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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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Project description:Psoriasis is one of the most common dermatological disorders, characterized by increased epidermal hyperplasia and immune cell infiltration. Psychological stress has been reported to contribute to the severity, aggravation, and relapse of psoriasis. We developed a chronic restrain stress (CRS)-imiquimod (IMQ)-induced psoriasis-like mouse model and performed a comprehensive comparative transcriptomic and metabolic analysis with control mice, CRS-treated mice, and IMQ-treated mice to investigate how psychological stress affects psoriasis. We found that CRS-IMQ-induced psoriasis-like mice showed significant exacerbation of psoriasis-like skin inflammation compared with mice treated with IMQ only. Mice of the CRS+IMQ group showed increased expression of keratinocyte proliferation and differentiation genes, differential regulation of cytokines, and promotion of the linoleic acid metabolism. Our study provides new insights into the effects of psychological stress on psoriasis pathogenesis and the mechanisms involved, which provides clues for development of therapeutics or biomarkers.

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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.

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