The mRNA expression analysis of mesenchymal stem cell from psoriasis skin lesion
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA428473 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6439910_1.fastq.gz | Fastqsanger.gz | |||
| SRR6439910_2.fastq.gz | Fastqsanger.gz | |||
| SRR6439905_1.fastq.gz | Fastqsanger.gz | |||
| SRR6439905_2.fastq.gz | Fastqsanger.gz | |||
| SRR6439906_1.fastq.gz | Fastqsanger.gz |
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Project description:mRNA sequencing for 6 samples of skin-derived mesenchymal stem cells from either normal skin or psoriasis skin lesion.
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Project description:RNA sequencing for 6 samples from psoriasis skin lesion mesenchymal stem cell, to examine the differentilly expressed mRNAs between two differernt conditions.
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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:To explore the cellullar and molecular alteration of human psoriasis, we collected full-thickness skin from the lesion region of 3 patients and the similar region of 3 healthy donors, and submit for single cell RNA sequencing (scRNAseq) with 10x genomics (V3.1). The transcriptional landscape of human psoriasis whole skin provide a unique view of immuno-regulation among skin cell types. 1. "Single cell transcriptional zonation of human psoriasis skin identifies an alternative immunoregulatory axis",<Cell Death Dis.>, 2021 May 6;12(5):450. https://yz-studio.shinyapps.io/shinyapph5ad/ 2. "Integrative single-cell transcriptomic investigation unveils long non-coding RNAs associated with localized cellular inflammation in psoriasis" <Front Immunol>2023 Sep 26:14:1265517. Integrated dataset: 106,675 cells from 11 healthy human skin and 79,887 cells from 9 psoriatic human skin https://yz-studio.shinyapps.io/psoriaticskincellatlas2/
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Project description:Applying ChIP-seq with anti-acetylation of lysine 27 on Histone 3 (H3K27Ac), we report high-throughput profiling of H3K27Ac in human skin biopsies taken from psoriasis patients, both from the lesion and from adjacent non-lesion skin, and from skin biopsies from healthy match volunteers, in term of age, gender, and the biopsies place in the body. From each group we had 4 samples. On three samples of each group we performed mRNA array. There is a clearly different H3K27 acetylation patterns in psoriatic skin compared to uninvolved or healthy volunteer skin. in many of the most over express genes in psoriasis lesion, there is enrichment of H3K27Ac. However, loss of acetylation on H3K27 is not part of the biochemical mechanism by which gene expression is decreased in psoriatic skin. Finally, we show Many of the over express genes in psoriasis lesion, that also were enriched with H3K27Ac harbor a putative GRHL transcription factor binding site.
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Project description:Psoriasis is a chronic inflammatory skin disease characterized by marked proliferation of keratinocytes leading to pronounced epidermal hyperplasia, elongation of rete ridges and hyperkeratosis. The most common form of psoriasis, chronic plaque psoriasis (Psoriasis vulgaris), involves relatively stable occurrence and progression of sharply demarcated lesions, usually on the trunk and extremities, which share a combination of trademark histological features, including tortuous and dilated dermal capillaries, loss of the epidermal granular layer, and accumulation of neutrophils beneath parakeratotic scale. In this study, whole-genome transcriptional profiling was used to characterize gene expression in 4 lesional and uninvolved skin samples obtained from patients with stable chronic plaque psoriasis. Skin mRNA expression was analysed by microarray. Four individuals with chronic plaque psoriasis were enrolled. 6 mm punch biopsies were obtained under local anaesthesia (lidocaine) from uninvolved skin and a target plaque.
2013-12-10 | E-GEOD-50790 | biostudies-arrayexpress
Project description:Ceramide is an important lipid in skin barrier function. Psoriasis is a chronic inflammatory skin disease, and the skin barrier function has disturbed. Furthermore, the balance of each ceramide species in stratum corneum is disrupted in psoriatic skin. However, it involved remains unclear what detailed mechanism ceramide species changed in psoriatic skin lesion. We comprehensively investigated lipid metabolism including ceramide in skin of psoriasis patients by DNA microarray analysis. The expression level of PNPLA1 gene involved in acylceramide synthesis which is epidermis-specific ceramide species essential for skin barrier function was decreased in psoriatic skin. In contrast, the expression level of lipid metabolism-related enzymes gene including ceramide were increased in psoriatic skin. Consequently, the acylceramide synthesis was decreased in skin of psoriasis patients, suggesting that increased biosynthesis of other sphingolipids to supplement the function of acylceramide may cause the pathology of psoriasis.
2024-03-16 | GSE168640 | GEO
Project description:Applying ChIP-seq with anti-acetylation of lysine 27 on Histone 3 (H3K27Ac), we report high-throughput profiling of H3K27Ac in human skin biopsies taken from psoriasis patients, both from the lesion and from adjacent non-lesion skin, and from skin biopsies from healthy match volunteers, in term of age, gender, and the biopsies place in the body. From each group we had 4 samples. There is a clearly different H3K27 acetylation patterns in psoriatic skin compared to uninvolved or healthy volunteer skin. in many of the most over express genes in psoriasis lesion, there is enrichment of H3K27Ac. However, loss of acetylation on H3K27 is not part of the biochemical mechanism by which gene expression is decreased in psoriatic skin. Finally, we show Many of the over express genes in psoriasis lesion, that also were enriched with H3K27Ac harbor a putative GRHL transcription factor binding site.
2023-07-17 | GSE161076 | GEO
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:Psoriasis is a chronic inflammatory skin disease characterized by marked proliferation of keratinocytes leading to pronounced epidermal hyperplasia, elongation of rete ridges and hyperkeratosis. The most common form of psoriasis, chronic plaque psoriasis (Psoriasis vulgaris), involves relatively stable occurrence and progression of sharply demarcated lesions, usually on the trunk and extremities, which share a combination of trademark histological features, including tortuous and dilated dermal capillaries, loss of the epidermal granular layer, and accumulation of neutrophils beneath parakeratotic scale. In this study, whole-genome transcriptional profiling was used to characterize gene expression in 4 lesional and uninvolved skin samples obtained from patients with stable chronic plaque psoriasis.Skin mRNA expression was analysed by microarray.
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