Transcriptome analysis of Psoriasis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA472389 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7192140.fastq.gz | Fastqsanger.gz | |||
| SRR7192150.fastq.gz | Fastqsanger.gz | |||
| SRR7192160.fastq.gz | Fastqsanger.gz | |||
| SRR7192131.fastq.gz | Fastqsanger.gz | |||
| SRR7192141.fastq.gz | Fastqsanger.gz |
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Project description:Characteization host-microbiome interactions in patients with allergic (model: atopic dermatitis) and autoimmune (model: psoriasis) diseases by integration of microarray transcriptome data with 16S microbial profiling. 6mm punch biopsies were collected from the skin of atopic dermatitis and psoriasis patients alongside healthy volunteers, and subjected to analysis using Affymetrix Human Gene ST 2.1 arrays.
2019-09-11 | E-MTAB-8149 | biostudies-arrayexpress
Project description:Purpose: The present study is aiming to understand transcriptome changes during psoriatic changes using high-throughput sequencing and thereby comprehensively assess the diseases and guide future research directions. Methods: Clinical psoriatic samples, including psoriatic lesions and their adjacent normal skin samples, and the surgical derived skins from healthy individuals as comparative controls were collected and analysed of their RNA expression profile using Illumina HiSeq 4000. raw sequencing reads were processed and pre-qualified using Trimmomatic and Fragments Per kb Per Million Reads (FPKM) method was used to calculate the abundance of each transcript followed by Negative Binomial Distribution tests to identify significant differences in each comparison. Results: Total reads for mRNAs, lncRNAs and miRNAs was 108,552, 105,136 and 2762, respectively, including 649 novel lncRNAs and 905 novel miRNAs. 5383 DE_mRNAs, 1201 DE_lncRNAs and 80 DE_miRNAs were identified in the comparison of the psoriasis lesions-adjacent normal group (PN) vs. healthy control-derived normal skin group (NN; PN vs. NN). A total of 9513 DE_mRNAs, 1940 DE_lncRNAs and 251 DE_miRNAs were identified in the psoriasis lesion group (PS) vs. NN comparison (PS vs. NN), and 4946 DE_mRNAs, 1559 DE_lncRNAs and 92 DE_miRNAs were identified in the PS vs. PN comparison. Conclusions: We identified numerous differentially expressed RNAs, including mRNAs, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs). Our results reveal transcriptomic changes, expand our mechanistic understanding of psoriasis, and may lead to new directions for psoriasis research.
2019-12-25 | GSE142582 | GEO
Project description:Although biomarker candidates associated with psoriasis have been suggested, those for predicting the risk of cardiovascular disease (CVD) early in patients with psoriasis are lacking. We aimed to identify candidate biomarkers that can predict the occurrence of CVD in psoriasis patients. We pursued quantitative proteomic analysis of serum samples composed of three groups: psoriasis patients with and those without CVD risk factors, and healthy controls. Age/Sex-matched serum samples were selected and labeled with 16-plex tandem mass tag (TMT) and analyzed using liquid chromatography-mass spectrometry and subsequent verification with ELISA. Of the 184 proteins that showed statistical significance (P-value <0.05) among the three groups according to TMT-based quantitative analysis, 98 proteins showed significant differences (>2.0-fold) between the psoriasis groups with and without CVD risk factors. Verification by ELISA revealed that caldesmon (CALD1), myeloid cell nuclear differentiation antigen (MNDA), and zyxin (ZYX) levels were significantly increased in the psoriasis group with CVD risk factors. Further network analysis identified pathways including integrin signaling, which could be related to platelet aggregation, and actin cytoskeleton signaling. Three novel candidates (MNDA, ZYX, and CALD1) could be potential biomarkers for predicting CVD risks in psoriasis patients. We expect these biomarker candidates can be used to predict CVD risk in psoriasis patients in clinical settings although further studies including large validation are needed.
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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.
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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.
2014-10-30 | PXD001387 | Pride
Project description:Oral Banzhilian Formula (BZLF) is effective in the clinical treatment of psoriasis. However, the effectiveness and mechanism of different drug delivery routes deserve further study. In this study, we externally applied BZLF to the skin lesions in an IMQ-induced psoriasis mice model, and found that BZLF alleviated the psoriasis-like skin lesions, while inhibiting the expression of Ki67 and inflammatory factors (Il17a, Tnf-α, S100a7 and Cxcl1) in the skin lesions. Finally, through transcriptome sequencing combined with bioinformatics and other methods, it was found that the mechanism of action of BZLF against psoriasis is achieved by down-regulating the LCN2/MMP-9 axis. Overall, this study elucidates the effectiveness and mechanism of external application of BZLF in the treatment of psoriasis, and provided a new approach and basis for clinical application.
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