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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The impact of the HSPA2 gene knockout on transcriptome profile in immortalized epidermal keratinocytes (HaCaT line)

ABSTRACT: The specific functional features of the epidermal keratinocytes are determined by the activity of many genes. The aim of the project was to characterize the role of HSPA2, a member of the HSPA chaperone family (HSP70), in human epidermal keratinocytes. The inactivation of the HSPA2 gene in the HaCaT line of spontaneously immortalized epidermal keratinocytes was performed by CRISPR/Cas9 gene editing system. Next, the effect of modifications on the transcriptomic profile of cells growing in a three-dimensional model of reconstructed human epidermis in vitro was investigated. The cells were grown at air-liquid interface culture on collagen-fibroblast matrix to achieve maximal level of HaCaT differentiation in RHE system.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Homo sapiens

SUBMITTER:

PROVIDER: E-MTAB-13166 | biostudies-arrayexpress |

SECONDARY ACCESSION(S): ERP149201

REPOSITORIES: biostudies-arrayexpress

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The impact of the HSPA2 gene knockout on transcriptome profile in immortalized epidermal keratinocytes (HaCaT line) grown in standard cell culture

Project description:The specific functional features of the epidermal keratinocytes are determined by the activity of many genes. The aim of the project was to characterize the role of HSPA2, a member of the HSPA chaperone family (HSP70), in human epidermal keratinocytes. The inactivation of the HSPA2 gene in the HaCaT line of spontaneously immortalized epidermal keratinocytes was performed by CRISPR/Cas9 gene editing system. Next, the effect of modifications on the transcriptomic profile of cells growing in 2D monolayer culture was investigated. This study was supported by a Polish National Science Center grant number NCN 2017/25/B/NZ4/01550.

2023-11-29 | E-MTAB-13251 | biostudies-arrayexpress

The impact of the HSPA2 gene downregulation on transcriptome profile in immortalized epidermal keratinocytes (HaCaT line) grown in 3D cell culture

Project description:The specific functional features of the epidermal keratinocytes are determined by the activity of many genes. The aim of the project was to characterize the role of HSPA2, a member of the HSPA chaperone family (HSP70), in human epidermal keratinocytes. The downregulation of HSPA2 gene in HaCaT cell line was performed by lentivirus-mediated shRNA method. Next, the effect of modifications on the transcriptomic profile of cells growing in a three-dimensional model of reconstructed human epidermis in vitro was investigated. The cells were grown at air-liquid interface culture on extracellular matrix to achieve maximal level of HaCaT differentiation in RHE system. This study was supported by a Polish National Science Center grant number NCN 2017/25/B/NZ4/01550.

2023-11-29 | E-MTAB-13266 | biostudies-arrayexpress

Transcriptomic analysis by AmpliSeq Ion Torrent to explore the effects of the long non-coding RNA TGFB2-AS1 on gene expression in human keratinocytes

Project description:TGFB2-AS1 is a long non-coding RNA which is induced by ΤGFβ signaling. In order to assess the importance of TGFB2-AS1 on the regulation of gene expression, we performed an AmpliSeq transcriptomic array in human keratinocytes (HaCaT), which stably over-express TGFB2-AS1 or control pcDNA3 empty vector. In addition, cells were stimulated with TGFβ1 for 24 hours, in order to observe the effects of TGFB2-AS1 on gene expression, downstream of TGFβ signaling. RNA from the following four conditions was used in this experiment: 1) pcDNA3, 2) pcDNA3+TGFβ1, 3) pcDNA3-TGFB2-AS1, 4) pcDNA3-TGFB2-AS1+TGFβ1. Biological triplicates were used per condition.

2019-07-01 | E-MTAB-7773 | biostudies-arrayexpress

Transcriptome profiling of MED1 wild-type and knockout human pre-B ALL cell line 697 (RNA-seq)

Project description:CRISPR/Cas9 system was used to generate mediator complex subunit 1 (MED1) knockout human pre-B ALL cell line 697. RNA-seq was performed to observe the effects of MED1 deletion on gene expression in 697.

2020-05-13 | E-MTAB-8178 | biostudies-arrayexpress

ZNF750 in late keratinocyte differentiation

Project description:Disrupted skin barrier due to altered keratinocyte differentiation is common in pathologic conditions such as atopic dermatitis, ichthyosis and psoriasis. However, the molecular cascades governing keratinocyte terminal differentiation are still poorly understood. We have previously demostrated that a dominante mutation in ZNF750 leads to a clinical phenotype that reminiscent of psoriasis and seborrehic dermatitis. We defined ZNF750 as a nuclear effector that is atrongly activated in and essiential for keratinocyte terminal differentiation. ZNF750 knockdown in HaCaT keratinocytes markedly reduced the expression of epidermal late differentiation markers, including gene subsets of epidermal differentiation complex and skin barrier formation such as FLG, LOR, SPINK5, ALOX12B and DSG1, known to be mutated in various human skin diseases. Furthermore, ZNF750 over-expression in undifferentiated cells induced terminal differentiation genes. Thus, ZNF750 is a regulator of keratinocyte terminal differnetiation, and with its downstream targets can serve in future elucidation of therapeutics for common disease of skin barrier Gene expression analysis: To determine the differentaition signature for HaCaT keratinocytes, with ZNF750 gene silencing, total RNA was isolated in biologic triplicates from cells induced to differentiate for twelve days and hybridized to Affymerix Human Gene 1.0 ST arrays.

2012-09-24 | E-GEOD-38039 | biostudies-arrayexpress

Mutant p63 affects epidermal cell identity through rewiring the enhancer landscape

Project description:<p>Transcription factor p63 is a key regulator of epidermal keratinocyte proliferation and differentiation. Mutations in the p63 DNA-binding domain are associated with Ectrodactyly Ectodermal Dysplasia Cleft Lip/Palate (EEC) syndrome. Underlying molecular mechanism of these mutations however remain unclear. Here we characterized the transcriptome and epigenome of p63 mutant keratinocytes derived from EEC patients. The transcriptome of p63 mutant keratinocytes deviated from the normal epidermal cell identity. Epigenomic analyses showed an altered enhancer landscape in p63 mutant keratinocytes contributed by loss of p63-bound active enhancers and by unexpected gain of enhancers. The gained enhancers were frequently bound by deregulated transcription factors such as RUNX1. Reversing RUNX1 overexpression partially rescued deregulated gene expression and the altered enhancer landscape. Our findings identify an unreported disease mechanism whereby mutant p63 rewires the enhancer landscape and affects epidermal cell identity, consolidating the pivotal role of p63 in controlling the enhancer landscape of epidermal keratinocytes.</p>

| phs001737 | dbGaP

Human keratinocytes HaCaT LC-MSMS_SDS exposure

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

Proteomic analysis of small extracellular vesicles (sEVs) derived from primary keratinocytes cultured in different calcium concentrations, treated with a peanut allergen extract and atopic dermatitis (AD)-relevant cytokines

Project description:Epidermal keratinocytes are key for maintenance of the integrity of the epidermis. One of the main drivers of keratinocyte differentiation is the calcium gradient; calcium concentration gradually increases towards the outer layers of the epidermis. Atopic dermatitis (AD) is a disorder associated with a chronic inflammatory state and a compromised epidermal barrier. Keratinocytes secrete lipid-rich small extracellular vesicles (sEVs) that acts as mediators of both local and long-distance signaling.

2022-06-07 | PXD031729 | Pride

Aberrantly expressed genes in HaCaT keratinocytes chronically exposed to arsenic trioxide

Project description:The purpose of this study is to search for aberrant genes in HaCaT keratinocytes after chronic exposure to arsenic trioxide. The objective of the investigation was to discover the mechanism of arsenic carcinogenicity in human epidermal keratinocytes. We hypothesize that a combined strategy of DNA microarray, qRT-PCR and gene function annotation will identify aberrantly expressed genes in HaCaT keratinocyte cell line after chronic treatment with arsenic trioxide. HaCaT cells were chronically exposed to 0.5M-BM-5g/mL arsenic trioxide (As2O3) up to 22 passages and RNA was extracted. Microarray data analysis identified 14 up-regulated genes and 21 down-regulated genes in response to arsenic trioxide Two experimental groups: 1. The treatment group was sub-cultured up to passage 22 to establish a chronic exposure state. 2. The passage control group was also sub-cultured up to 22 passages but with no exposure to arsenic trioxide. 4 technical replicates with 3 replicates making a total of 8X3 =24 samples HaCat Cell untreated (passage control): 1. H1_H001, H1_H002, H1_H003 2. H2_ H004, H2_H005, H2_H006 3. H3_ H007, H3_H008, H3_H009 4. H4_ H010, H4_H011, H4_H012 HaCat Cell treated with 0.5M-BM-5g/ml of arsenic trioxide: 5. A1_H013, A1_H014, A1_H015 6. A2_H016, A2_H017, A2_H018 7. A3_H019, A3_H020, A3_H021 8. A4_H022, A4_H023, A4_H024 Cell Type: Human Skin Keratinocyte: 1.5 M-CM-^W105 HaCaT cells were cultured in 7.5 ml of complete DMEM containing 10% Fetal Bovine Serum (FBS) and 1% penicillin, streptomycin in T-25 culture plate. Cells were incubated in a humidified atmosphere with 5% CO2 at 37 M-BM-:C. The treatment groups were exposed to 0.5M-BM-5g/mL As2O3 (equivalent to LC 0.5), and passaged at 90% confluent. Total RNA was extracted from 4 technical replicates of unexposed HaCaT cells and HaCaT cells chronically exposed to arsenic trioxide up to passage 22 using RNA STAT-60 (TEL-TEST, INC, Friendswood, TX, USA).

2012-04-11 | E-GEOD-37192 | biostudies-arrayexpress

Systemic perturbation of keratinocyte homeostasis

Project description:We performed comprehensive proteome profiling (ECM and cell lysate) of human collagen VII deficient and control epidermal keratinocytes to generate global and detailed images of dysregulated epidermal molecular pathways linked to loss of collagen VII. These revealed downregulation of interaction partners of collagen VII, but also increased abundance of S100 pro-inflammatory proteins and enhanced activity of lysosomal proteases. Thus, loss of a single extracellular structural protein, collagen VII, induced persistent fibrosis enabling inflammatory and tissue destabilizing activities of keratinocytes.

2018-01-16 | PXD005873 | Pride

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