Effects of REDD1 KO in transcriptomic response to wounding and glucocorticoid treatment in HaCaT human keratinocytes
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PROVIDER: PRJNA736990 | ENA |
REPOSITORIES: ENA
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Project description:REDD1 KO affects basal global gene expression profile and transcriptomic response to wounding and glucocorticoid treatment in HaCaT human keratinocytes
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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.
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Project description:The keratinocyte cell line HaCaT was cultured for three days (proliferation) or for ten days (differentiation). RNA from cells at day3 was compared to RNA from cells at day10. The microarray hybridizations were performed in dye-swap procedure : RNA from cells at day3 was labeled with Cy3 (GSM4674, GSM4675, GSM4682, GSM4683) and then with cy5 (GSM4680, GSM4681). Keywords = cell density differentiation program in human keratinocytes
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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.
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Project description:Triton X-100 has been used as a model substance to study the effects of irritants on the skin. HaCaT human keratinocyte cell line were treated with a non-cytotoxic dose of Triton X-100, as determined by the MTT assay and microscopically examination) for 48 h. The altered abundance of proteins from HaCaT keratinocytes exposed to Triton X-100 was analyzed by LC-MS/MS approach and quantified using Progenesis LC software.
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Project description:The keratinocyte cell line HaCaT was cultured for three days (proliferation) or for ten days (differentiation). RNA from cells at day3 was compared to RNA from cells at day10. The microarray hybridizations were performed in dye-swap procedure : RNA from cells at day3 was labeled with Cy3 (GSM4674, GSM4675, GSM4682, GSM4683) and then with cy5 (GSM4680, GSM4681). Keywords = cell density differentiation program in human keratinocytes Keywords: repeat sample
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Project description:Dendritic epidermal T cells (DETC) reside in murine skin and participate in homeostasis and wound repair. Upon wounding, DETC become activated through the recognition of an unidentified ligand expressed by keratinocytes proximal to sites of injury. Such DETC activation is mediated through a monoclonal T cell receptor (TCR). Using a soluble form of this monoclonal TCR, we have shown that keratinocytes upregulate DETC TCR ligands in wounded tissue within 2 hours following wounding. Down-modulation of the ligand is seen 3 hours following wounding, and no expression is evident in non-wounded skin. In vitro studies on cell lines which express this unknown ligand indicate that antigen recognition by the DETC TCR is dependent upon N-linked glycosylation of the ligand. Given the glycosylation sensitivity of the ligand and the restricted expression following wounding, we are interested in pursuing microarray analysis to identify genes that are modulated in keratinocytes in response to wounding.
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