The miRNA microarray data after UVB exposure to human keratinocyte HaCaT cells
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ABSTRACT:
PROVIDER: PRJNA597340 | ENA |
REPOSITORIES: ENA
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Project description:UVB plays a key role in inflammation and DNA damage in human skin. Human keratinocyte HaCaT cells were utilized to determine the up- and down-regulated miRNA after UVB exposure. We used microarrays to identify the miRNA affected after UVB (15 mJ/cm^2) exposure to HaCaT cells
2020-03-23 | GSE142534 | GEO
Project description:Background: The biological functions of HA are related to its molecular weight and binding to its receptor TLR4 or CD44. Recent studies have shown that LMW-HA exhibits proinflammatory effects, while HMW-HA functions as an anti-inflammatory factor. UVB-induced epidermal inflammation is mainly mediated by endogenous molecules, such as DAMPs, that cause severe skin damage by activating TLR signaling pathways. Objective: Since both LMW- and HMW-HA have inhibitory functions on TLR-mediated macrophage inflammation, HA is assumed to suppress UVB-induced DAMP-mediated inflammation in the skin. In this study, both uLMW-HA and HMW-HA were found to inhibit UVB-induced keratinocyte inflammation. Methods: To elucidate whether HAs have anti-inflammatory effects on inflammation induced by UVB exposure, we performed whole transcriptome analysis in HaCaT cells treated with or without HAs after UVB exposure. Results: UV radiation induced upregulation or downregulation of genes (FC>1.2 or FC<0.8, q<0.05) were obtained. We analyzed network of these genes with Ingenuity Pathway analysis using information collected from databases on protein interactions. IL-6 was detected as an upstream factor of HA suppressing UV-radiation effects on HaCaT cells. Canonical pathway analysis also shows uLMW-HA downregulated NF-κB, which is located downstream of TLR4 signaling pathway, although HMW-HA did not show downregulation of NF-κB signaling pathway. Conclusions: Both uLMW-HA and HMW-HA were found to inhibit UVB-induced keratinocyte inflammation.
2022-08-05 | GSE201850 | GEO
Project description:Purpose: To compare the transcriptomes of UVB (20mJ/cm2 and 40mJ/cm2) exposed and untreated HaCaT keratinocytes by RNA-Seq analysis, trying to find differences in gene expression between UVB exposed and untreated of keratinocytes and then elucidate the candidate genes that may play important roles in the differentiation of UVB-induced damage in keratinocytes. Methods: HaCaT keratinocytes were subjected to 20mJ/cm2 and 40mJ/cm2 UVB irradiation. Results: To better understand the effects of UVB (20 mJ/cm2), mRNA-sequecing (n=3) were completed by Novogene Inc. A total 891 differentially expressed genes (DEGs) were identified between UV group and control group with 604 down-regulated and 287 up-regulated. A total of 4036 differentially expressed genes (DEGs) which compared with untreated group were identified by RNA-Seq, which provided abundant data for further analysis.
2019-10-12 | GSE138800 | GEO
Project description:Cell density affects keratinocyte behaviors and gene expression. Here, We examines the differential expressed genes regulated by cell density. We performed RNA-seq analysis to compare HaCaT cells cultured under high- or low0density conditions. The Gene Ontology Biological Process terms enriched among differential expressed genes through DESeq2 included cell adhesion and keratinocyte differentiation. Our data provides the understanding of keratinocyte behavior regulated by cell density.
2024-07-04 | GSE247733 | GEO
Project description:Ultraviolet B (UVB) light is a common environmental trigger that can induce flares in several autoimmune diseases. Here, we modeled photosensitivity in mice which express an autoimmune-driving isoform of Foxp3 without the second coding exon of the gene, called FoxP3ΔE2 mice. In the steady-state, FoxP3ΔE2mice generate keratinocyte-specific IgE autoantibodies and more autoreactive T follicular helper (TFH) cells that target keratinocyte-derived autoantigens that are released upon exposure to damaging doses of UVB. After UVB light challenge in vivo, FoxP3ΔE2mice generated more IgE antibodies, increased germinal center formation, had higher percentages of IL-4+TFHs, developed worsened skin pathology and had higher concentrations of IgE in UVB-damaged skin. We also observed a significant increase in IgE on basophils and accumulation of basophil extracellular traps in UVB-challenged skin of FoxP3ΔE2mice. Collectively, FoxP3ΔE2mice fail to maintain self-tolerance in GCs, causing IgE autoantibody production and driving exaggerated photosensitivity.
2024-11-14 | GSE247794 | GEO
Project description:We employed human HaCaT cells as a model system to identify cellular proteins that accompany SDS-induced toxicity based on a proteomic approach. HaCaT human keratinocyte cell line were treated with a non-cytotoxic dose of SDS (25 µg/ml, as determined by the MTT assay and microscopically examination) for 48 h. The altered abundance of proteins from HaCaT keratinocytes exposed to SDS was analyzed by LC-MS/MS approach and quantified using Progenesis LC software. The abundance of 217 proteins (which were identified by multiple peptides, ≥ 2) was altered in keratinocytes exposed to SDS; in which 131 proteins had increased abundance while 86 proteins was down regulated. The Pathview map of 131 up-regulated proteins was built and enhancement of glycolysis/gluconeogenesis was found.
2017-11-03 | PXD007789 | Pride
Project description:To address CPD-dependent UVB activities, a model system was established in which transfection of keratinocytes with pseudouridine-modified mRNA (M-NM-(-mRNA) encoding CPD-photolyase resulted in 90% reduction of CPDs within 6 and 24 hours after UVB exposure. Microarray analysis of this model system demonstrated that more than 50 % of the gene expression altered by UVB were changed in a CPD-dependent manner. The expression of most of the CPD-dependent genes was changed at 6 h after UVB as compared to 24 h likely due to the higher CPD levels. Nine genes (ATF3, CCNE1, CDKN2B, EGR1, ID2, PTGS2, RUNX1, SNAI1, SNAI2) regulated by CPDs were selected for further investigation (qPCR, Western blot) based on the microarray data. Gene expression modulated by UVB irradiation in HaCaT keratinocytes was measured at 6 and 24 hours after the exposure to dose of 20 mJ/cm2 UVB. Three independent experiments were performed at each time (6 or 24 hours) using different passages for each experiment.
2015-01-16 | E-GEOD-65034 | biostudies-arrayexpress
Project description:Aim of the study was to characterize at a molecular level (changes in transcriptomes) the effect of monosodium urate crystal (MSU) on HaCaT keratinocyte cell line. This was adressed by using a culture model. The HaCaT cell line (human keratinocytes) was stimulated by MSU (1mg/mL) vs control for 12 hrs. By using genome-wide expression profiling, we identified deregulation of functionally relevant gene networks. HaCaT were obtained from Cell Lines Service (Eppelheim, Germany) and grown in DMEM medium (PAN biotech, Aidenbach, Germany) supplemented with 10% FBS (Life Technology, Grand Island, NY, USA), L-glutamine and non-essential amino acid. Before the treatment HaCaT cells were cultured in serum-free medium for 12hrs. HaCaT were treated with MSU (1mg/ml) vs DMEM control for 12hrs then submitted to RNA extration and gene expression profiling. Triplicate experiments were performed: HaCaT control (n=3), MSU-treated (n=3).
2015-10-29 | E-GEOD-65931 | biostudies-arrayexpress
Project description:The present study was designed to use small interfering RNA (siRNA) approach to identify the effects of NCSTN silencing on human immortal keratinocyte cell line, HaCaT. The alteration of gene expression profiles after NCSTN gene silencing in HaCaT cells was investigated employing Agilent whole genome microarray
2018-04-28 | GSE68346 | GEO
Project description:Aim of the study was to characterize at a molecular level (changes in transcriptomes) the effect of monosodium urate crystal (MSU) on HaCaT keratinocyte cell line. This was adressed by using a culture model. The HaCaT cell line (human keratinocytes) was stimulated by MSU (1mg/mL) vs control for 12 hrs. By using genome-wide expression profiling, we identified deregulation of functionally relevant gene networks.
2015-10-29 | GSE65931 | GEO