Keratinocyte-derived circulating exosomal miRNAs as a novel biomarker of disease severity in psoriasis
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ABSTRACT:
PROVIDER: PRJNA888960 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21850582.fastq.gz | Fastqsanger.gz | |||
| SRR21850583.fastq.gz | Fastqsanger.gz | |||
| SRR21850584.fastq.gz | Fastqsanger.gz | |||
| SRR21850585.fastq.gz | Fastqsanger.gz | |||
| SRR21850586.fastq.gz | Fastqsanger.gz |
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Project description:To reveal the relationship between circulating exosomal miRNAs and the disease severity of psoriasis, we performed next-generation sequencing from plasma exosomes of patients with high psoriasis area and severity index (PASI) score (>10) and low PASI score (<5). We identified 19 differentially expressed exosomal miRNAs that were significantly different between the groups. We validated the top three up-and down-regulated exosomal miRNAs using quantitative real-time PCR.
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Project description:Background: The role of serum extracellular vesicles (EVs) are less known in psoriasis. Objectives: To explore the transcriptomic profile of serum EVs and the potential biomarkers in psoriasis. Methods: EVs were isolated by differential ultracentrifugation and identified by transmission electron microscope. The diameters of EVs were detected using nanoparticle tracking analysis. Serum EVs-keratinocyte interaction was observed through confocal fluorescence microscopy. miRNA microarray and mRNA microarray were performed in serum EVs (n=4) and skin lesions (n=3), respectively. qRT-PCR and fluorescence in situ hybridization were used to detect the expression of miRNAs in serum EVs and skin lesions (n=15). Bioinformatics analysis was performed to predict the potential target genes and functions of miR-1305 and miR-6785-5p. Western blot, CCK-8 and Elisa were used to detect the EVs’ biomarkers, keratinocytes proliferation and cytokines secretion. Results: A total of 16 miRNAs and 1,725 mRNAs were significantly dysregulated in serum EVs and skin lesions, respectively. miR-1305 was downregulated and miR-6785-5p was upregulated both in serum EVs and skin lesions. Serum EVs could be uptaken by keratinocytes. MiR-1305 was downregulated and miR-6785-5p were upregulated in keratinocytes after cocultured with psoriasis serum EVs compared with controls. Psoriasis serum EVs promoted keratinocytes proliferation and the secretion of CCL20 and IL-8. Serum EVs miR-1305 and miR-6785-5p were associated with disease severity. Conclusions: Serum EVs might be involved in the activation of keratinocytes through loaded miRNAs in psoriasis. Serum EVs miR-1305 and miR-6785-5p can be served as biomarkers of psoriasis.
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Project description:miR-378a regulates keratinocyte responsiveness to IL-17A in psoriasis
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Project description:We report the high-throughput profiling of human primary keratinocytes transfected with either miR-378 mimic or miR-378 inhibitor at 24 or 48 hours. Our study focused on the dysregulation of microRNAs that might partially be a fundamental mechanism leading to psoriasis development. We knock-in and knock-out a specific miR-378 and see the cellular responses. As expected, overexpression of miR-378a inhibited the proliferation, enhanced the apoptosis and disturbed the cell cycle. Regarding to the confirm experiment, our results suggested that the expression of miR-378a associated with the psoriasis pathogenesis enhancing the severity of psoriatic lesion, and might useful for further development of therapeutic strategy for psoriasis.
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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:Disrupted skin barrier due to altered keratinocyte differentiation is common in pathologic conditions such as atopic dermatitis, ichthyosis and psoriasis. However, the molecular cascades governing keratinocyte terminal differentiation are still poorly understood. We have previously demostrated that a dominante mutation in ZNF750 leads to a clinical phenotype that reminiscent of psoriasis and seborrehic dermatitis. We defined ZNF750 as a nuclear effector that is atrongly activated in and essiential for keratinocyte terminal differentiation. ZNF750 knockdown in HaCaT keratinocytes markedly reduced the expression of epidermal late differentiation markers, including gene subsets of epidermal differentiation complex and skin barrier formation such as FLG, LOR, SPINK5, ALOX12B and DSG1, known to be mutated in various human skin diseases. Furthermore, ZNF750 over-expression in undifferentiated cells induced terminal differentiation genes. Thus, ZNF750 is a regulator of keratinocyte terminal differnetiation, and with its downstream targets can serve in future elucidation of therapeutics for common disease of skin barrier Gene expression analysis: To determine the differentaition signature for HaCaT keratinocytes, with ZNF750 gene silencing, total RNA was isolated in biologic triplicates from cells induced to differentiate for twelve days and hybridized to Affymerix Human Gene 1.0 ST arrays.
2012-09-24 | E-GEOD-38039 | biostudies-arrayexpress
Project description:Disrupted skin barrier due to altered keratinocyte differentiation is common in pathologic conditions such as atopic dermatitis, ichthyosis and psoriasis. However, the molecular cascades governing keratinocyte terminal differentiation are still poorly understood. We have previously demonstrated that a dominant mutation in ZNF750 leads to a clinical phenotype that reminiscent of psoriasis and seborrheic dermatitis. We defined ZNF750 as a nuclear effector that is strongly activated in and essential for keratinocyte terminal differentiation. ZNF750 knockdown in HaCaT keratinocytes markedly reduced the expression of epidermal late differentiation markers, including gene subsets of epidermal differentiation complex and skin barrier formation such as FLG, LOR, SPINK5, ALOX12B and DSG1, known to be mutated in various human skin diseases. Furthermore, ZNF750 over-expression in undifferentiated cells induced terminal differentiation genes. Thus, ZNF750 is a regulator of keratinocyte terminal differentiation, and with its downstream targets can serve in future elucidation of therapeutics for common disease of skin barrier
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Project description:Scalp psoriasis shows a variable clinical spectrum and in many cases poses a great therapeutic challenge. However, it remains unknown whether the immune response of scalp psoriasis differs from understood pathomechanisms of psoriasis on other skin areas. We sought to determine the cellular and mollecular phenotype of scalp psoriasis by performing a comparative analysis of scalp vs skin using lesional and nonlesional samples from 20 Caucasian subjects with untreated moderate to severe psoriasis and significant scalp involvement, and 10 control subjects without psoriasis. Our results suggest that even in the scalp psoriasis is a disease of the inter-follicular skin. The immune mechanisms that mediate scalp psoriasis were found to be similar to those involved in skin psoriasis. However, the magnitude of dysregulation, number of differentially expressed genes, and enrichment of the psoriatic genomic fingerprinting were more prominent in skin lesions. Furthermore, the scalp transcriptome showed increased modulation of several gene-sets, particularly those induced by interferon-gamma, compared with skin psoriasis which was mainly associated with activation of TNFâµ/L-17/IL-22-induced keratinocyte response genes. We also detected differences in expression of gene-sets involving negative regulation, epigenetic regulation, epidermal differentiation, and dendritic cell or Th1/Th17/Th22-related T-cell processes. To define the transcriptomic profile of scalp skin, punch biopsies (6 mm diameter) were obtained from 20 Caucasian patients with untreated moderate to severe psoriasis with significative scalp involvement and 10 control subjects without psoriasis (N). Lesional (LS) samples were isolated from the infiltrated border of a plaque of psoriasis. Non lesional (NL) samples were taken from scalp areas with no visible psoriasis between the infiltrated plaques.
2015-11-25 | E-GEOD-75343 | biostudies-arrayexpress
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.
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