H3K27Ac modification and gene expression in psoriasis
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ABSTRACT:
PROVIDER: PRJNA674860 | ENA |
REPOSITORIES: ENA
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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. 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: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.
2021-01-01 | GSE160932 | 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.
2014-10-30 | PXD001387 | Pride
Project description:We analyzed m6A modifications in skin lesions of patients with psoriasis or atopic dermatitis (AD). The results of this study will help to gain insight into the molecular basis of m6A modification in inflammatory skin diseases such as psoriasis or atopic dermatitis.
2024-08-20 | GSE268744 | GEO
Project description:Development of gene expression signatures for psoriasis
| PRJNA751566 | ENA
Project description:Silencing of MED13L impairs Mediator-regulated chromatin H3K27ac modification in NSCLC. Here, we performed H3K27ac ChIP-seq to investigate impacts of miR-4497 or knocking-down MED13L on chromatin H3K27ac modification in NSCLC PC9 cells.
2020-08-19 | GSE147120 | GEO
Project description:Psoriasis is a Tcell-mediated disease characterized by the chronic inflammation of skin. Gene expression analyses on skin biopsies and freshly isolated PBMCs have provided important insights into Psoriasis pathophysiology. In the present study we analyze, for the first time, the gene expression profile of in vitro activated T cells in Psoriasis compared to normal heatlhy controls.
2013-12-02 | GSE47598 | GEO
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:To further explore the gene expression signatures in psoriatic, we have employed whole genome microarray expression profiling as a discovery platform to identify the potential genes that play a role in the pathogenesis of psoriasis. 3 psoriasis specimens were collected from patients with psoriasis and 3 normal skin were obtained from cosmetic surgeries as controls.The analysis identified a set of 4956 differentially expressed circRNAs，2194 significantly dysregulated lncRNAs，and 1725 discrepant mRNAs .Among all the differential expressed circRNAs, 3016 upregulated circRNAs and 1940 downregulated circRNAs were found in psoriatic lesions compared with normal healthy skin tissues.
2021-08-03 | GSE181318 | GEO
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