LIGHT induces psoriais and atopic dermatitis related genes in keratinocyte
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ABSTRACT:
PROVIDER: PRJNA937601 | ENA |
REPOSITORIES: ENA
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Project description:LIGHT upregulated a varity of genes in the human keratinocytes that are found to be highly expressed in the patients with psoriais and atiopic dermatitis. RNA was isolated from 3 different replicates per group, using a Qiagen kit and subjected to RNA-seq analysis.
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Project description:Atopic dermatitis, which is a common inflammatory skin disease characterized by persistent epidermal barrier dysfunction, is a systemic health burden reducing overall quality of life of the person. Recently, we showed that the nonstructural extracellular matrix molecule Thrombospondin-4 (THBS4) was upregulated in psoriatic skin lesions by more than 2-fold. In addition, THBS4 contributed to both skin regeneration and wound healing in vitro and in vivo. In the present work we found that THBS4 is also abundantly expressed in atopic dermatitis (AD) patient skin biopsies. By using a proteotransciptomic approach we show that stimulation of primary keratinocytes with THBS4 activates multiple factors, including inflammation, migration, proliferation, keratinocyte differentiation, by which THBS4 could participate in AD progression and contribute to the wound healing process.
2025-03-29 | PXD037593 | Pride
Project description:Atopic dermatitis is increasing worldwide, correlating with air pollutions. Various organic components of pollutants activate transcription factor AhR (aryl-hydrocarbon receptor). We have established AhR-CA mice, whose keratinocytes express constitutive-active AhR, and these mice developed atopic dermatitis-like frequent scratching and allergic inflammation. In this study we performed ChIP-seq analyses and identified keratinocyte-specific AhR target genes, including inflammatory cytokines Tslp and IL33, and neurotrophic factor Artemin. While AhR-CA mice exhibited epidermal hyperinnervation and alloknesis leading to hypersensitivity to pruritus, blockade of Artemin alleviated these phenotypes. AhR-CA mice showed scratching-induced barrier insufficiency and enhanced sensitization to epicutaneously-applied antigens, recapitulating human atopic dermatitis. Consistently, AhR activation and Artemin expression was detected in the epidermis of atopic dermatitis patients and keratinocytes exposed to air pollutants. Thus, AhR in keratinocytes senses the environmental stimuli and responds to them through moderating inflammation. We propose a mechanism in which air pollution induces atopic dermatitis through AhR activation.
2016-11-13 | GSE72449 | GEO
Project description:Recently, it was shown that lesional skin of atopic dermatitis patients expresses low levels of some antimicrobial peptides, compared with psoriasis patients. Here we performed microarray analysis on mRNA from purified lesional epidermal cells of patients with chronic plaque psoriasis and chronic atopic dermatitis, to investigate whether this is a general phenomenon for host defense proteins, and how specific it is for this class of molecules. We found overexpression of many antimicrobial genes in keratinocytes from psoriatic skin compared with atopic dermatitis skin. Interestingly, we observed that markers of normal differentiation and the activated/hyperproliferative epidermal phenotype were expressed at equal levels. Chronic lesions of psoriasis and atopic dermatitis patients are remarkably similar with respect to cellular proliferation. We conclude that psoriatic epidermis expresses high levels of host defense proteins compared with atopic dermatitis epidermis, and this phenomenon appears to be specific for these proteins. It remains to be investigated whether this is caused by genetic polymorphisms in pathways leading to an epidermal antimicrobial response, or by differences in the cellular infiltrate in psoriasis compared with atopic dermatitis. In general the microarray technique is used to probe a (very large) number of genes for say the deseased and the healthy state.Then gene ontology is used to detect the involved pathways.We did not set out to find a comprehensive list of genes involved in these skin deseases.We do suspect that the "path way" approach might be a bit anthropomorphic.Here we offered a different approach.We set out to investigate the evolutionary fitness changes from one local maximum , Psoriasis , to another , Atopie. Our hypothesis is that Psoriasis is at one extreme in the reaction of the evolution to invading micro organisms and Atopie at an other.So the vast chemical web called human being with numorous feedback and feed forward signals would then be tilted a bit in multidimensional Gene Space and the microarray technique would show us a glimpse of the involved genes. Keywords: Disease state analysis
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Project description:Atopic Dermatitis (AD) is the most common inflammatory skin disease and characterized by a deficient epidermal barrier and cutaneous inflammation. Genetic studies suggest a key role of keratinocytes in AD pathogenesis, but the alterations in the proteome that occur in the entire epidermis have not been defined. Employing a pressure-cycling technology-data-independent acquisition (PCT-DIA) approach, we performed quantitative proteomics of epidermis from healthy volunteers and lesional and non-lesional skin of AD patients. Results were validated by targeted proteomics using parallel reaction monitoring mass spectrometry or by immunofluorescence staining. The identified proteins reflect the strong inflammation in lesional skin and the defect in keratinocyte differentiation and epidermal stratification. Most importantly, they reveal impaired activation of the NRF2-antioxidant pathway and reduced abundance of mitochondrial proteins involved in key metabolic pathways in the epidermis. These results provide insight into the molecular alterations in the epidermis of AD patients and identify novel targets for pharmaceutical intervention.
2022-10-04 | PXD025431 | Pride
Project description:mRNA array analysis of total RNA from primary kertinocytes from three healthy controls, three atopic dermatitis patients and three psoriasis patients was carried out
2012-06-01 | E-MTAB-728 | biostudies-arrayexpress
Project description:In this study we used genomic profiling to characterize differences in expression of genes related to epidermal growth/differentiation and inflammatory circuits in skin lesions of psoriasis and atopic dermatitis (AD), comparing expression values to normal skin. Skin biopsies were collected from 9 patients with chronic atopic dermatitis, 15 psoriasis patients, and 9 healthy volunteers. Keywords: Genetic-pathology Psoriasis and AD are common inflammatory skin diseases which share important features, including: 1) large infiltrates of T-cells and inflammatory dendritic cells in skin lesions, 2) immune activation with up-regulated expression of many cytokines, chemokines, and inflammatory molecules 3) marked epidermal hyperplasia in chronic diseased skin and 4) defective barrier function with increased transepidermal water loss (TEWL), which reflects underlying alterations in keratinocyte differentiation. Using genomic profiling we provide a comprehensive comparison of chronic psoriasis and AD skin lesions as compared with normal skin.
2009-10-31 | E-GEOD-16161 | biostudies-arrayexpress
Project description:TWEAK Upregulates atopic dermatitis related genes
| PRJNA885774 | ENA