The role of keratinocyte DDX5 in IMQ-induced psoriatic mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE208671 | GEO | 2022/10/24
REPOSITORIES: GEO
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Project description:The role of keratinocyte DDX5 in IMQ-induced psoriatic mice
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Project description:Psoriasis is a systemic disease with cutaneous manifestations. MicroRNAs (miRNAs) are non-coding RNA molecules that are differentially expressed in psoriatic skin, however; only few miRNAs have been localized to specific cells or regions of psoriatic lesions. We used laser capture microdissection (LCM) and next-generation sequencing to study the specific miRNA expression profiles in the epidermis (Epi) and dermal inflammatory aggregates (RD/ICs) of psoriatic skin. We identified 24 deregulated miRNAs in the Epi and 37 deregulated miRNAs in the RD/ICs of lesional psoriatic skin compared with non-lesional psoriatic skin (FCH>2, FDR<0.05). Interestingly, 9 of the 37 miRNAs, including miR-193b and miR-223 that have recently been described as deregulated in circulating peripheral blood mononuclear cells (PBMCs) from patients with psoriasis. Using flow cytometry and qRT-PCR, miR-193b and miR-223 were found to be expressed in Th17 cells. In conclusion, we demonstrate that LCM combined with small RNA sequencing provides a robust strategy to explore the global miRNA expression in the epidermal and dermal compartments of psoriatic skin. Furthermore, our results indicate that the altered local miRNA changes seen in the RD/ICs is reflected in the circulating immune cells, altogether emphasizing that miRNAs may contribute to a systemic component in the pathogenesis of psoriasis. Examination of the global miRNA expression in epidermis (Epi) and dermis (RD/ICs) of paired (non-lesional vs. lesional) psoriatic skin using a combination of laser-capture microdissection and barcoded small RNA sequencing
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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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