Dissecting the miRNome of psoriatic keratinocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA531085 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8858250.fastq.gz | Fastqsanger.gz | |||
| SRR8858260.fastq.gz | Fastqsanger.gz | |||
| SRR8858251.fastq.gz | Fastqsanger.gz | |||
| SRR8858261.fastq.gz | Fastqsanger.gz | |||
| SRR8858252.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The purpose of this study was to identify the miRNome of keratinocytes in psoriasis Method: We performed next-generation sequencing for small RNAs from the RNA samples obtained from keratinocytes from psoriasis lesional, non-lesional and healthy skin. Next, we removed adapters and the low quality tags from the sequencing data and clean reads were mapped and aligned to known miRNAs sequences (miRBase 21). Novel miRNA transcripts were predicted based on the length (22-25 nucleotide) and secondary structure (precursor analysis) using MIREAP and mapped to the human genome. Data were normalized (transcripts per million, TPM) and analysed using Bioconductor-EdgeR. Group comparisons (lesional vs. healthy, lesional vs. non lesional and non-lesional vs. healthy) were performed. MiRNAs with <10% FDR, fold change >1.4 (1 TPM at least in one of the groups and expressed in half of the samples in any group) were considered statistically significant. Results: Robust expression of 411 known and 30 novel miRNAs (TPM > 1 in >50% of the samples in at least one of the groups) was detected in our samples. Using EdgeR we identified 104 miRNAs with significantly altered level (fold change > 1.4, FDR < 0.1) between healthy and psoriatic keratinocytes (P vs H). While, pair-wise comparison of miRNA expression in keratinocytes from non-lesional and lesional psoriasis skin (P vs. N) identified 87 deregulated miRNAs. Comparison of the miRNome of keratinocytes from non-lesional skin of psoriasis patients to healthy keratinocytes (N vs. H) identified 7 differentially expressed miRNAs. Conclusion: Here, for the first time we show the keratinocyte miRNome in psoriasis which may serve as the basis for future functional studies of miRNAs deregulated in keratinocytes in psoriasis.
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Project description:The aim of the study was to investigate the apoptotic process in psoriatic keratinocytes. UV radiation was used as apoptosis stimuli. Restults provide insights into the role of UV radiation and apoptosis induction on cultured psoriatic keratinocytes compared to healthy controls.
2017-01-12 | GSE93423 | GEO
Project description:The psoKC (psoriatic keratinocyte) model is represnting the behavour of keratinocytes in the later or chronic stage of psoriasis in response to the main cytokines that constitute the characteristic cytokine milieu, namely IFNg and TNFa (mainly derived by Th1 cells), and IL-17 and IL-22 (mainly derived by Th17 cells).
Additionally, the model explores the role of exogenous PGE2 through the activation of EP4 receptor signaling. The response to the aforementioned stimuli was not only limited to the cell fate decisions of keratinocytes (proliferation, apoptosis or differentiation) but also include their effect on the psoriatic environment with respect to the secretion of ligands and intercellular-acting stimuli.
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Project description:To investigate the function of the NET-AIM2 axis on keratinocyte activation during psoriasis, we established psoriatic NETs-treated primary human keratinocytes in which AIM2 has been knocked down by siRNA
2022-10-28 | GSE216519 | GEO
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.
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Project description:Next to genetic alterations, it is being recognized that the cellular environment also acts as a major determinant in onset and progression of disease. In cases where different cell types contribute to the final disease outcome, this imposes environmental challenges as different cell types likely differ in their extracellular dependencies. A number of skin diseases, including psoriasis is characterized by a combination of keratinocyte hyperproliferation and immune cell activation. Activation of immune cells involves increased glucose consumption thereby intrinsicly limiting glucose availability for other cell types. Thus, these type of skin diseases require metabolic adaptations that enable coexistence between hyperproliferative keratinocytes and activated immune cells in a nutrient-limited environment. Hsa-microRNA-31-5p (miR-31) is highly expressed in keratinocytes within the psoriatic skin. Here we show that miR-31 expression in keratinocytes is induced by limited glucose availability and enables increased survival of keratinocytes under limiting glucose conditions, by increasing glutamine metabolism. In addition, miR-31 induced glutamine metabolism results in secretion of specific metabolites (aspartate and glutamate) but also secretion of immuno-modulatory factors. We show that this miR-31-induced secretory phenotype is sufficient to induce Th17 cell differentiation, a hallmark of psoriasis. Inhibition of glutaminase (GLS) using CB-839 impedes miR31-induced metabolic rewiring and secretion of immuno-modulatory factors. Concordantly, pharmacological targeting of GLS alleviated psoriasis pathology in a mouse model of psoriasis. Together our data illustrate an emerging concept of metabolic interaction across cell compartments that characterizes disease development, which can be employed to design effective treatment options for disease, as shown here for psoriasis.
2023-02-06 | PXD029030 | Pride
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: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 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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