Expression data of keratinocytes from condyloma acuminata and skin tissues
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE140662 | GEO | 2020/03/11
REPOSITORIES: GEO
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Project description:Expression data of keratinocytes from condyloma acuminata and skin tissues
| PRJNA590482 | ENA
Project description:The aim of this study was to analyze the in vitro biological epidermal processes occurring in reconstructed skins using cells from breast skin of African and Caucasian skin type color. A exploration of mRNA expression levels in the epidermis of reconstructed skin was undertaken to elucidate the differential in vitro functions of keratinocytes. The reconstruction of skin models was made with keratinocytes and fibroblasts from four different donors per skin type and experiments were conducted in triplicate for each donor. At the end of culture, the epidermis from reconstructed skin was manually separated from the dermal equivalent part in order to analyse gene expression in keratinocytes only. RNA samples were labelled with biotin and hybridation was performed on Affymetrix Human Genome U133 + PM Array Plates.
2020-08-10 | E-MTAB-9433 | biostudies-arrayexpress
Project description:Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from human skin keratinocytes derived from healthy donors, as well as from telomerase immortalised human skin keratinocytes (N/TERT), transduced with mock, EGFP, or EGFP-GLI2DeltaN transgenes to compare chromosomal ploidy status. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from human skin keratinocytes derived from healthy donors, as well as from telomerase immortalised human skin keratinocytes (N/TERT) to compare chromosomal ploidy status
2012-02-28 | E-GEOD-36105 | biostudies-arrayexpress
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 | GSE72455 | GEO
Project description:Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from human skin keratinocytes derived from healthy donors, as well as from telomerase immortalised human skin keratinocytes (N/TERT), transduced with mock, EGFP, or EGFP-GLI2DeltaN transgenes to compare chromosomal ploidy status.
2012-02-28 | GSE36105 | GEO
Project description:Recent study has revealed that long non-coding RNAs (lncRNAs) perform as important regulators of cellular physiology and pathology, which makes them promising therapeutic and diagnostic entities. We found lncRNA WAKMAR1 is significantly down-regulated in wound-edge keratinocytes from venous ulcer and diabetic foot ulcer compared to the normal wounds. To study the genes regulated by WAKMAR1, we transfected lncRNA GapmeRs into human primary epidermal keratinocytes to inhibit its expression. We performed a global transcriptome analysis of keratinocytes upon inhibition of WAKMAR1 using Affymetrix arrays. We performed a global transcriptome analysis of keratinocytes upon inhibition of WAKMAR1 using Affymetrix arrays.
2018-05-26 | GSE114908 | GEO
Project description:The morphology and the behavior of skin and oral tissue keratinocytes are different. One significant dissimilarity between the two sites is the response to injury. Oral and skin keratinocytes have intrinsic differences in the response to injury and such differences are reflected in gene expression profiles. We used microarrays to investigate differences in global gene expression patterns between baseline skin and oral epithelium sheets without their underlying connective tissue.
2014-06-15 | GSE56135 | GEO
Project description:The aim of our study was to explore lncRNA expression profile in keratinocytes of patients with psoriasis vulgaris to provide new insights into psoriasis.
2023-02-28 | GSE146149 | GEO
Project description:The morphology and the behavior of skin and oral tissue keratinocytes are different. One significant dissimilarity between the two sites is the response to injury. Oral and skin keratinocytes have intrinsic differences in the response to injury and such differences are reflected in gene expression profiles. We used microarrays to investigate differences in global gene expression patterns between baseline skin and oral epithelium sheets without their underlying connective tissue. Paired skin and oral epithelium was separated from the dermis for RNA extraction and hybridization on Affymetrix microarrays. Skin epidermal tissues were obtained from the tail of mice and oral epidermal tissues were obtained from the hard palate. Enzymatically isolated epithelium was used for analysis.
2014-06-15 | E-GEOD-56135 | biostudies-arrayexpress
Project description:The DEAD-box (DDX) proteins function in diverse cellular processes including RNA alternative splicing, and are linked to immune-mediated diseases. However, little is known about the roles of DDXs in skin inflammatory diseases. Here, we show that DDX5, one of the founding members of the DDX RNA helicase family, controls skin inflammation and participates in the pathogenesis of psoriasis via regulating IL-36R pre-mRNA splicing. We found that both mRNA and protein of DDX5 are decreased in lesional skin from patients with psoriasis and psoriasis-like mice, and that mice with keratinocyte-specific ablation of DDX5 spontaneously develop psoriasis-like phenotypes. Mechanistically, DDX5 complexes with serine/arginine-rich splicing factor 1(SRSF1) to typically regulate IL-36R pre-mRNA splicing in keratinocytes, which generates mRNAs encoding full-length IL-36R and a previously unknown soluble form of IL-36R (sIL-36R). sIL-36R controls IL-36/IL-36R signaling by competing with IL-36R for IL-36γ ligation. The reduction or deficiency of DDX5 leads to IL-36R pre-mRNA splicing preferring to the generation of IL-36R but not sIL-36R, thereby selectively amplifying inflammatory responses of keratinocytes to IL-36γ and then aggravating cutaneous inflammation in psoriasis. Genetic restoration or intradermal administration of sIL-36R in psoriasis-like mice suppresses IL-36R signaling and alleviates the disease phenotype of psoriasis. Altogether, these data reveal a pathogenic role of DDX5 during psoriasis, and provide mechanistic insights into the regulation of IL-36R splicing and its impact on psoriasis development.
2020-09-09 | PXD021379 |