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Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE97306 | GEO | 2018/01/23

REPOSITORIES: GEO

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Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure [miRNA]

Project description:Determining the miRNA and mRNA expression profiles in HaCaT cells at early and late stages of arsenite exposure to reveal early and late changes in the HaCaT cells transformation process.

2018-01-23 | GSE97305 | GEO

Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure [mRNA]

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Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure [miRNA-seq]

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Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure (RNA-Seq)

2021-07-07 | GSE107054 | GEO

Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure

Project description:Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure

| PRJNA381230 | ENA

Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure [miRNA-seq]

Project description:Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure [miRNA-seq]

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Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure (RNA-Seq)

Project description:Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure (RNA-Seq)

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Protein dataset of immortalized keratinocyte HaCaT cells and normal human keratinocytes.

Project description:Learning of the molecular mechanisms of the pathological processes development in the normal human keratinocytes (NHK) are difficult. Immortalized keratinocytes HaCaT are often used as an analogue of NHK since they have a number of advantages over the latter - they do not require the presence of growth and differentiation factors in the medium, have unlimited potential for proliferation, demonstrate stable phenotype regardless of the number of passages [1]. Taking into account the properties and characteristics of the HaCaT line, these cells can be considered as a promising experimental model for research of various physiological processes occurring in human keratinocytes. However, to understand the limitations of such an experimental model, a detailed comparative characterization of HaCaT and NHK is required, which can be obtained by carrying out its proteomic analysis. In this article we present datasets obtained through the high-throughput shotgun proteomics analysis of normal human keratinocytes and immortalized HaCaT keratinocytes. As a protocol for proteomic profiling of cells, we used the approach of obtaining LC-MS / MS measurements followed by their processing with Progenesis LC-MS software (Nonlinear Dynamics Ltd.). The mzML files were deposited to the Mendeley Data.

| S-EPMC7921465 | biostudies-literature

Protein dataset of immortalized HaCaT cells p53 knock down HaCaT keratinocytes

Project description:The p53 protein is encoded by TP53 gene and plays the key role in significant number of cellular processes including proliferation, apoptosis and regulation of many stress response pathways. P53 acts like a direct transcription activator of numerous genes regulating cell cycle arrest, DNA repair, growth inhibition and many others (Mollereau and Ma, 2014). The canonical biological function of p53 is maintaining genome integrity via elimination of damaged or exposed to genotoxic stress cells. Immortalized HaCaT cells are widely used for keratinocyte research, since they maintain stable keratinocyte phenotype, have nearly unlimited proliferative potential, do not require specific growth and differentiation factors (Colombo et al., 2017). Also, HaCaT cells produce typical differentiation markers such as cytokeratins K14 and K10, involucrin (Colombo et al., 2017) and respond to keratinocyte differentiation stimuli. Taking together, HaCaT cells have similar to normal human keratinocytes (NHK) properties, however, as many of spontaneously immortalized cell lines HaCaT cells bear two mutant p53 alleles - R282Q and H179Y (Lehman et al., 1993). Mutp53 in HaCaT has an increased affinity to other p53 family members (p63, p73), which significantly expands p53 properties. Moreover, mutp53 indirectly affects specific target genes via protein-protein interactions with other transcription factors (NF-Y, E2F1, NF-KB) or by tethering p63 to new promotor locations. For more detailed investigation of mutp53 impact on various processes in HaCaT cells we performed a shRNA mediated knockdown of mutp53. For generation of stable TP53 knockdown we employed plasmid vector pLKO-p53-shRNA-941 (Addgene # #25637) followed by puromycin selection of transduced cells. Here we present proteomic dataset obtained from wild type HaCaT cells and p53 knock down HaCaT keratinocytes.

2022-04-28 | PXD033538 | Pride

PCB153 reduces telomerase activity and telomere length in immortalized human skin keratinocytes (HaCaT) but not in human foreskin keratinocytes (NFK).

Project description:Polychlorinated biphenyls (PCBs), ubiquitous environmental pollutants, are characterized by long term-persistence in the environment, bioaccumulation, and biomagnification in the food chain. Exposure to PCBs may cause various diseases, affecting many cellular processes. Deregulation of the telomerase and the telomere complex leads to several biological disorders. We investigated the hypothesis that PCB153 modulates telomerase activity, telomeres and reactive oxygen species resulting in the deregulation of cell growth. Exponentially growing immortal human skin keratinocytes (HaCaT) and normal human foreskin keratinocytes (NFK) were incubated with PCB153 for 48 and 24days, respectively, and telomerase activity, telomere length, superoxide level, cell growth, and cell cycle distribution were determined. In HaCaT cells exposure to PCB153 significantly reduced telomerase activity, telomere length, cell growth and increased intracellular superoxide levels from day 6 to day 48, suggesting that superoxide may be one of the factors regulating telomerase activity, telomere length and cell growth compared to untreated control cells. Results with NFK cells showed no shortening of telomere length but reduced cell growth and increased superoxide levels in PCB153-treated cells compared to untreated controls. As expected, basal levels of telomerase activity were almost undetectable, which made a quantitative comparison of treated and control groups impossible. The significant down regulation of telomerase activity and reduction of telomere length by PCB153 in HaCaT cells suggest that any cell type with significant telomerase activity, like stem cells, may be at risk of premature telomere shortening with potential adverse health effects for the affected organism.

| S-EPMC3288560 | biostudies-literature

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