Co-Morbid Multiple Sclerosis and Psoriasis: Clinical Outcomes and Gene Expression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA594859 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Psoriasis was found to ameliorate multiple sclerosis (MS) outcomes when it MS onset. However, the molecular basis for this observation remains unclear. Herein, we compared the blood mononuclear cell transcriptome of psoriasis and MS comorbide (P/MS) patients with that of patients with either psoriasis or MS to understand the clinical observation.
2020-12-11 | GSE141804 | GEO
Project description:ICLIC-MS for Enhancing Outcomes Research and Clinical Care in Multiple Sclerosis
| PRJNA848916 | ENA
Project description:Anti-TNF-alpha therapy has made a significant impact on the treatment of psoriasis. Despite being designed to neutralize TNF-alpha activity, the mechanism of action of these agents in the resolution of psoriasis remains unclear. The aim of this study was to better understand the mechanism of action of etanercept by examining very early changes in the lesional skin of psoriasis patients. 20 chronic plaque psoriasis patients were enrolled and received 50mg etanercept twice weekly. Skin biopsies were obtained before treatment and on days 1, 3, 7 and 14 post-treatment. Skin mRNA expression was analysed by microarray. Twenty individuals with chronic plaque psoriasis were enrolled (age range 18-75 years). Entry criteria included age greater than 18 years and stable plaque-type psoriasis involving at least 10% body surface area. Exclusion criteria included use of systemic psoriasis therapy within 4 weeks, topical therapy within 2 weeks, or severe co-morbid diseases. For 12 weeks, subjects received etanercept (Enbrel) 50mg twice a week subcutaneously. At baseline, 6 mm punch biopsies were obtained under local anaesthesia (lidocaine) from uninvolved skin and a target plaque. Subsequent biopsies were taken on days 1, 3, 7 and 14 of therapy from the same target plaque.
2014-06-07 | E-GEOD-47751 | biostudies-arrayexpress
Project description:This study was carried out to determine how immunological signatures related in the colon and periperhal blood between indivudals with Crohn's, Spondyloarhtritis, and individuals with both diseases. We carried out one experiments with 1 patient in each condition (1 Crohn's, 1 Spondyloarthritis, 1 Co-morbid, 1 HC), which we then repeated for a total of 8 subjects.
2021-05-25 | GSE163314 | GEO
Project description:Background: Psoriasis is a chronic disease characterized by the development of scaly red skin lesions and possible co-morbid conditions. The psoriasis lesional skin transcriptome has been extensively investigated, but mRNA levels do not necessarily reflect protein abundance. Methods: Lesional (PP) and uninvolved (PN) skin samples from 14 patients were analyzed using high-throughput complementary DNA sequencing (RNA-seq) and liquid chromatography-tandem mass spectrometry (LC-MS/MS). Results: We identified 4122 differentially expressed genes (DEGs) along with 748 differentially expressed proteins (DEPs). Global shifts in mRNA were modestly correlated with changes in protein abundance (r = 0.40). We identified similar numbers of increased and decreased DEGs, but 4-fold more increased than decreased DEPs. Ribosomal subunit and translation proteins were elevated within lesions, without a corresponding shift in mRNA expression (RPL3, RPS8, RPL11). We identified 209 differentially expressed genes/proteins (DEGPs) with corresponding trends at the transcriptome and proteomic levels. Most DEGPs were similarly altered in at least one other skin disease. Psoriasis-specific and non-specific DEGPs had distinct cytokine-response patterns, with only the former showing disproportionate induction by IL-17A in cultured keratinocytes. Conclusions: Our findings reveal global imbalance between the number of increased and decreased proteins in psoriasis lesions, consistent with heightened translation. This effect could not have been discerned from mRNA profiling data alone. We have also identified high-confidence DEGPs and shown that only those most specific to psoriasis are enriched with IL-17A targets. RNA-seq-based comparison between gene expression in psoriasis lesions and uninvolved skin from 14 patients
2015-08-23 | E-GEOD-67785 | biostudies-arrayexpress
Project description:To understand the mechanism of disease progression in psoriasis, we defined Asian small plaque psoriasis (small psoriasis) and Asian intermediate plaque psoriasis (intermediate psoriasis) as psoriasis subtypes with limited disease progression, and compared their cellular and molecular signatures with the classic subtype of Western large plaque psoriasis (large psoriasis; GSE30999). Transcriptome analyses in pre-treatment skin biopsies from patients with Asian small and intermediate plaque psoriasis. 12 Asian small plaque psoriasis skin biopsy tissues (7 lesional and 5 non-lesional skin) and 15 Asian intermediate plaque psoriasis skin biopsy tissues (7 lesional and 8 non-lesional skin). GCRMA (using gcrma package from R/Bioconductor) and adjusted for batch effect. The expression data was combined with Western large psoriasis (GSE30999). Using a normalization based upon quantiles, the expression data was normalized based upon a specified normalization distribution of GSE30999 (see publication for GSE67853). The complete dataset representing: (1) 12 Asian small plaque psoriasis Samples, (2) 15 Asian intermediate plaque psoriasis Samples, and (3) 130 Western large plaque psoriasis Samples from GSE30999 (re-processed), is linked below as a supplementary file.
2016-01-10 | E-GEOD-67853 | 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:To understand the mechanism of disease progression in psoriasis, we defined Asian small plaque psoriasis (small psoriasis) and Asian intermediate plaque psoriasis (intermediate psoriasis) as psoriasis subtypes with limited disease progression, and compared their cellular and molecular signatures with the classic subtype of Western large plaque psoriasis (large psoriasis; GSE30999).
2016-01-10 | GSE67853 | GEO
Project description:Comparing Co-morbid Crohn's-Spndyloarhtritis to each of the underlying dieases
| PRJNA685745 | ENA
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