RNA sequencing of psoriasis and healthy keratinocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1147211 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30248700_1.fastq.gz | Fastqsanger.gz | |||
| SRR30248700_2.fastq.gz | Fastqsanger.gz | |||
| SRR30248701_1.fastq.gz | Fastqsanger.gz | |||
| SRR30248701_2.fastq.gz | Fastqsanger.gz | |||
| SRR30248702_1.fastq.gz | Fastqsanger.gz |
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Project description:Psoriasis is a common chronic inflammatory skin disease determined by genetic and environmental factors, resulting in IL-23/IL-17-mediated immune activation and epidermal hyperproliferation and activation. Here, we performed RNA sequencing of CD45-negative epidermal cells from psoriasis lesions and healthy skin to characterize the landscape of coding and non-coding transcripts in keratinocytes in psoriasis and healthy skin.
2025-02-18 | GSE274560 | GEO
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.
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Project description:Psoriasis is a common chronic inflammatory skin disease. Keratinocytes (KCs) are important effector cells that can recruit inflammatory cells by releasing inflammatory factors and chemokines to promote the inflammatory cascade in psoriasis. However, the mechanism underlying KC activation in psoriasis remains unclear. Livin is an inhibitor of apoptotic proteins and its expression can directly affect the proliferation and metastasis of tumor cells. Livin expression has been reported to be significantly increased in the lesions of patients with psoriasis; however, its specific role in KC activation has not yet been reported. The aim of this study was to investigate whether livin regulates KC activation and causes the release of inflammatory mediators. The expression levels of livin in patients with psoriasis, an imiquimod (IMQ) mouse model, and M5-treated HaCaT cells were determined via immunofluorescence staining, reverse transcription-quantitative polymerase chain reaction, enzyme-linked immunosorbent assay (ELISA), and western blotting. We constructed livin knockdown (Knockdown-HaCaT) and negative control (NC-HaCaT) cells using human immunodeficiency virus-1-based lentiviral vectors to study the function of livin in KCs via RNA-sequencing and proteomics analysis. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed. Moreover, the effect of livin expression on the release of inflammatory mediators in KCs was verified using ELISA.
2024-05-22 | PXD035174 | Pride
Project description:In 2019, our group performed small RNA-sequencing on keratinocytes isolated from lesional and non-lesional psoriasis skin as well as from healthy skin, and identified miRNAs with altered levels in psoriasis keratinocytes (Srivastava et al., 2019). One of the miRNAs we identified to be overexpressed in psoriasis keratinocytes was miR-378a-3p. In this study, we aimed to explore the regulation and function of miR-378a in keratinocytes and its potential role in psoriasis. We used microarrays to identify differentially expressed genes upon miR-378a overexpression in primary human keratinocytes as part of the study and gain insights about the modulation of specific pathways.
2021-03-08 | GSE164400 | GEO
Project description:Single-cell RNA sequencing is transforming how we understand skin immunology, but previous human skin single-cell RNA sequencing data included only a small fraction of inflammatory cells among the overall cell population, such that functional subsets may be difficult to ascertain. We have overcome these obstacles by harvesting inflammatory cells emigrating from a half of 6 mm punch biopsy skin after 48-hour incubation in culture medium without any enzyme, and then analyzing the harvested cells with single-cell RNA sequencing. By this strategy, we obtained single-cell RNA sequencing data of 24,354 cells (leukocytes 46.0%, keratinocytes 49.6%, and melanocytes 2.4%) from 13 human psoriasis skin and 5 healthy volunteer skin. Unsupervised clustering identified NK cells, CD161+ T-cells, CD8+ T-cells, CD4+ T-cells, regulatory T-cells, mature & semimature dendritic cells, melanocytes, and keratinocytes in different layers - S. (Stratum) corneum, S. granulosum, S. spinosum, and S. basale. To understand psoriasis immunopathogenesis at single-cell levels, we compared gene expression between psoriasis cells vs. control cells within each inflammatory cell subtype clusters.
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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 our study was to explore lncRNA expression profile in keratinocytes of patients with psoriasis vulgaris to provide new insights into psoriasis.
2023-02-28 | GSE146149 | GEO
Project description:The immunopathogenesis of psoriasis, a common chronic inflammatory disease of the skin, is incompletely understood. Here we demonstrate, using a combination of single cell and spatial RNA sequencing, IL-36 dependent amplification of IL-17A and TNF inflammatory responses in the absence of neutrophil proteases, which primarily occurred within the supraspinous layer of the psoriatic epidermis. We further show that a subset of SFRP2+ fibroblasts in psoriasis contribute to amplification of the immune network through transition to a pro-inflammatory state. The SFRP2+ fibroblast communication network involves production of CCL13, CCL19 and CXCL12, connected by ligand-receptor interactions to other spatially proximate cell types: CCR2+ myeloid cells, CCR7+ LAMP3+ dendritic cells, and CXCR4 expressed on both CD8+ Tc17 cells and keratinocytes, respectively. The SFRP2+ fibroblasts also express cathepsin S, further amplifying inflammatory responses by activating IL-36G in keratinocytes. These data provide an unprecedented view of psoriasis pathogenesis, which expands our understanding of the critical cellular participants to include inflammatory fibroblasts and their cellular interactions.
2023-05-07 | GSE225475 | GEO
Project description:Herein we demonstrate the efficacy of an unbiased proteomics screening approach for studying protein expression changes in the KC-Tie2 psoriasis mouse model, identifying multiple protein expression changes in the mouse and validating these changes in human psoriasis. KC-Tie2 mouse skin samples (n=3) were compared with littermate controls (n=3) using gel-based fractionation followed by label-free protein expression analysis. 5482 peptides mapping to 1281 proteins were identified and quantitated: 105 proteins exhibited fold-changes ≥2.0 including: stefin A1 (average fold change of 342.4 and an average P = 0.0082; cystatin A, human orthologue); slc25a5 (average fold change of 46.2 and an average P = 0.0318); serpinb3b (average fold change of 35.6 and an average P = 0.0345; serpinB1, human orthologue); and kallikrein related peptidase 6 (average fold change of 4.7 and an average P = 0.2474; KLK6). We independently confirmed mouse gene expression-based increases of selected genes including serpinb3b (17.4-fold, P < 0.0001), KLK6 (9.0-fold, P = 0.002), stefin A1 (7.3-fold; P < 0.001) and slc25A5 (1.5-fold; P = 0.05) using qRT-PCR on a second cohort of animals (n=8). Parallel LC/MS/MS analyses on these same samples verified protein-level increases of 1.3-fold (slc25a5; P < 0.05), 29,000-fold (stefinA1; P < 0.01), 322-fold (KLK6; P < 0.0001) between KC-Tie2 and control mice. To underscore the utility and translatability of our combined approach, we analyzed gene and protein expression levels in psoriasis patient skin and primary keratinocytes vs. healthy controls. Increases in gene expression for slc25a5 (1.8-fold), cystatin A (3.0-fold), KLK6 (5.8-fold) and serpinB1 (76-fold; all P < 0.05) were observed between healthy controls and involved lesional psoriasis skin and primary psoriasis keratinocytes. Moreover slc25a5, cystatin A, KLK6 and serpinB1 protein were all increased in lesional psoriasis skin compared to normal skin. These results highlight the usefulness of preclinical disease models using readily-available mouse skin and demonstrate the utility of proteomic approaches for identifying novel peptides/proteins that are differentially regulated in psoriasis that could serve as sources of auto-antigens or provide novel therapeutic targets for the development of new anti-psoriatic treatments.
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Project description:PLA2G4D is a phospholipase and transacylase expressed in epidermal keratinocytes, and its expression is upregulated in inflammatory skin disorders such as psoriasis. Treatment of primary keratinocytes with proinflammarory cytokines IL17A and TNFα markedly increases Pla2g4d-mRNA expression. To investigate the function of PLA2G4D, we conducted bulk RNA sequencing of primary keratinocytes isolated from wild-type and Pla2g4d-deficient mice and studied transcriptional changes under basal and cytokine stimulation. The sequencing data suggests that PLA2G4D modulates fundamental biological processes including cell proliferation, differentiation, and signaling.
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