Combined miRNA-mRNA transcriptional profiling in the human skin [mRNA_PSOR]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE145304 | GEO | 2020/12/07
REPOSITORIES: GEO
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Project description:mRNA and miRNA transcription changes during epidermal differentiation and between lesional psoriatic skin and normal skin were analyzed
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Project description:mRNA and miRNA transcription changes during epidermal differentiation were analysed using proliferating keratinoctes (pKC), differentiated keratinocytes (dKC) and skin equivalents (SE)
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Project description:mRNA and miRNA transcription changes during epidermal differentiation were analysed using proliferating keratinoctes (pKC), differentiated keratinocytes (dKC) and skin equivalents (SE)
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Project description:Psoriasis is a systemic disease with cutaneous manifestations. MicroRNAs (miRNAs) are non-coding RNA molecules that are differentially expressed in psoriatic skin, however; only few miRNAs have been localized to specific cells or regions of psoriatic lesions. We used laser capture microdissection (LCM) and next-generation sequencing to study the specific miRNA expression profiles in the epidermis (Epi) and dermal inflammatory aggregates (RD/ICs) of psoriatic skin. We identified 24 deregulated miRNAs in the Epi and 37 deregulated miRNAs in the RD/ICs of lesional psoriatic skin compared with non-lesional psoriatic skin (FCH>2, FDR<0.05). Interestingly, 9 of the 37 miRNAs, including miR-193b and miR-223 that have recently been described as deregulated in circulating peripheral blood mononuclear cells (PBMCs) from patients with psoriasis. Using flow cytometry and qRT-PCR, miR-193b and miR-223 were found to be expressed in Th17 cells. In conclusion, we demonstrate that LCM combined with small RNA sequencing provides a robust strategy to explore the global miRNA expression in the epidermal and dermal compartments of psoriatic skin. Furthermore, our results indicate that the altered local miRNA changes seen in the RD/ICs is reflected in the circulating immune cells, altogether emphasizing that miRNAs may contribute to a systemic component in the pathogenesis of psoriasis. Examination of the global miRNA expression in epidermis (Epi) and dermis (RD/ICs) of paired (non-lesional vs. lesional) psoriatic skin using a combination of laser-capture microdissection and barcoded small RNA sequencing
2015-04-01 | E-GEOD-57012 | biostudies-arrayexpress
Project description:In this study, we sought to establish the usefulness of LCM on cDNA microarray analysis. We reported that LCM samples improved the sensitivity of detection of differentially expressed genes over conventional bulk tissue analysis. We also provided the new information of chemokine and its receptor interaction within psoriatic lesional skin. For the comparison of gene expression patterns between single and double amplification techniques, total RNA was extracted from blocks of paired lesional and non-lesional psoriatic skin biopsies from four patients. For LCM experiment, total RNA was extracted from sliced tissue sections of paired lesional and non-lesional psoriatic skin biopsies from three patients.
2012-01-30 | E-GEOD-26866 | biostudies-arrayexpress
Project description:The efficacy of monoclonal antibodies against either interleukin (IL)-17 or the IL-17 receptor in psoriasis therapy provides strong evidence that IL-17 is the major inflammatory mediation in this disease. However, how IL-17 induces epidermal hyperplasia in psoriasis remains largely unknown. Here, we show that IL-17 actives NF-kB in keratinocytes and initiates the NF-kB-dependent transcription of microRNA-31 (miR-31), one of the most abundant microRNAs in the epidermis of lesional skin of psoriasis and two related mouse models. Similar to IL-17 deficiency (IL-17-/-), knocking out miR-31 (miR-31-/-) or targeting it by antagomir-31 prevents keratinocytes Ki67 expression and inhibits acanthosis and dermal inflammation in psoriasis mouse model. Moreover, PPP6c, a negative regulator restricting G0/G1 to G2/M phase progression in the cell cycle, is diminished in human psoriatic epidermis and is directly targeted by miR-31. Inhibition of ppp6c is functionally important for the biological effects of miR-31 in the development of epidermal hyperplasia. Thus, our data define IL-17-inducede miR-31 and its target ppp6c as critical factors for hyperproliferative epidermis in psoriasis. Epidermis samples from affected ears derived from 3 CD18hypo PL/J mice (DIS) or normal ears derived from 3 CD18hypo C57BL/6J mice(2128) were used for RNA extraction and hybridization on Affymetrix microarrays. We sought to compare miRNA expression of normal skin from control and lesional skin.
2013-12-31 | E-GEOD-50099 | biostudies-arrayexpress
Project description:Psoriasis is a systemic disease with cutaneous manifestations. MicroRNAs (miRNAs) are non-coding RNA molecules that are differentially expressed in psoriatic skin, however; only few miRNAs have been localized to specific cells or regions of psoriatic lesions. We used laser capture microdissection (LCM) and next-generation sequencing to study the specific miRNA expression profiles in the epidermis (Epi) and dermal inflammatory aggregates (RD/ICs) of psoriatic skin. We identified 24 deregulated miRNAs in the Epi and 37 deregulated miRNAs in the RD/ICs of lesional psoriatic skin compared with non-lesional psoriatic skin (FCH>2, FDR<0.05). Interestingly, 9 of the 37 miRNAs, including miR-193b and miR-223 that have recently been described as deregulated in circulating peripheral blood mononuclear cells (PBMCs) from patients with psoriasis. Using flow cytometry and qRT-PCR, miR-193b and miR-223 were found to be expressed in Th17 cells. In conclusion, we demonstrate that LCM combined with small RNA sequencing provides a robust strategy to explore the global miRNA expression in the epidermal and dermal compartments of psoriatic skin. Furthermore, our results indicate that the altered local miRNA changes seen in the RD/ICs is reflected in the circulating immune cells, altogether emphasizing that miRNAs may contribute to a systemic component in the pathogenesis of psoriasis.
2015-04-01 | GSE57012 | GEO
Project description:Epidermal hyperplasia, a characteristic feature of psoriatic skin lesions, is epigenetically driven by Enhancer of Zeste homolog 2 (EZH2). EZH2 and EZH2-mediated trimethylation of histone H3 lysine 27 (H3K27me3) are both abnormally upregulated in psoriatic lesions. To identify microRNAs that could potentially target these epigenetic regulators we profiled miRNAs from psoriatic lesional skin in comparison with healthy skin. Analysis of the differentially expressed miRNAs revealed miR-101, as one of the most significant miRNA, consistently downregulated in psoriatic lesions compared to the healthy skin. A clear inverse correlation in the expression of miR-101 versus EZH2 was apparent in normal skin versus psoriatic lesional skin indicating that EZH2 is a potential target of miR-101, which was further confirmed by luciferase assay. Investigating the upstream effectors of the miR-101- EZH2 pathway in psoriasis, we identified the pro-inflammatory cytokine IL-17 as regulator of miR-101 expression. Here we propose a model, depicting a pathway triggered by IL-17 – mediated modulation of miR-101 expression, which in turn elicit sustained expression of EZH2, leading to enhanced keratinocyte proliferation and epidermal hyperplasia in psoriasis. Taken together, this indicates that miR-101 is a potential therapeutic target to alleviate the downstream effects of IL-17 mediated epidermal hyperplasia in psoriasis.
2023-09-19 | GSE220586 | GEO
Project description:Background: Plaque psoriasis is a chronic autoimmune disorder characterized by the development of red scaly plaques. To date psoriasis lesional skin transcriptome has been extensively studied, whereas only few proteomic studies of psoriatic skin are available. Aim: The aim of this study was to compare protein expression patterns of lesional and normally looking skin of psoriasis patients with skin of the healthy volunteers, reveal differentially expressed proteins and identify changes in cell metabolism caused by the disease. Methods: Skin samples of normally looking and lesional skin donated by psoriasis patients (n = 5) and samples of healthy skin donated by volunteers (n = 5) were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). After protein identification and data processing, the set of differentially expressed proteins was subjected to protein ontology analysis to characterize changes in biological processes, cell components and molecular functions in the patients' skin compared to skin of the healthy volunteers. Results: The performed analysis identified 405 and 59 differentially expressed proteins in lesional and normally looking psoriatic skin compared to healthy control. We discovered decreased expression of KNG1, APOE, HRG, THBS1 and PLG in normally looking skin of the patients. Presumably, these changes were needed to protect the epidermis from spontaneous activation of kallikrein-kinin system and delay the following development of inflammatory response. In lesional skin, we identified several large groups of proteins with coordinated expression. Mainly, these proteins were involved in different aspects of protein and RNA metabolism, namely ATP synthesis and consumption; intracellular trafficking of membrane-bound vesicles, pre-RNA processing, translation, chaperoning and degradation in proteasomes/immunoproteasomes. Conclusion: Our findings explain the molecular basis of metabolic changes caused by disease in skin lesions, such as faster cell turnover and higher metabolic rate. They also indicate on downregulation of kallikrein-kinin system in normally looking skin of the patients that would be needed to delay exacerbation of the disease.
2021-05-06 | PXD021673 | Pride
Project description:Atopic dermatitis (AD) is a common inflammatory skin disease with underlying defects in epidermal function and immune responses. The goal of this study was to investigate differences in gene expression in lesional skin from patients with mild extrinsic or intrinsic AD compared to skin from healthy controls and from lesional psoriasis skin. The aim was to identify differentially expressed genes involved in skin barrier formation and inflammation, and to compare our results with those reported for patients with moderate and severe AD. A total of 31 samples were analyzed: 8 healthy skin, 9 psoriatic plaques, 4 extrinsic AD lesional skin, 10 intrinsic AD lesional skin.
2016-03-08 | E-GEOD-75890 | biostudies-arrayexpress