Similar Datasets
Project description:Tranexamic acid may promote melanocores clustering in keratinocytes through upregulation of Rab5b
| PRJNA856499 | ENA
Project description:Targets of Retinoic Acid (RA) and 3,4-didehydroretinoic acid (ddRA) were identified in primary human epidermal keratinocytes grown in the presence of atRA or ddRA for 4 and 24 hours. Retinoids (natural forms and synthetic derivatives of vitamin A) are used as therapeutic agents for numerous skin diseases such as keratinization disorders (e.g. ichthyoses) and psoriasis. Two endogenous ligands for retinoic acid receptors exist, retinoic acid (atRA) and 3,4-didehydroretinoic acid (ddRA). In primary human epidermal keratinocytes many transcriptional targets for atRA are known, whereas the targets for ddRA are unknown. In an attempt to determine the targets, we compared the effect of atRA and ddRA on transcriptional profiles in undifferentiated and differentiating human primary keratinocytes. First, as expected, many genes were induced or suppressed in response to keratinocyte differentiation. Furthermore, the two retinoids affected substantially more genes in differentiated keratinocytes (more than 350) than in proliferating keratinocytes (20). In differentiating keratinocytes markers of cornification were suppressed suggesting a de-differentiating effect by the two retinoids. When comparing the expression profile of atRA to that of ddRA, no differently regulated genes were found. The array analysis also found that a minor number of miRNAs and a large number of non-coding transcripts were changed during differentiation and in response to the two retinoids. Furthermore, the expression of all, except one, genes known to cause autosomal recessive congenital ichthyosis (ARCI) were found to be induced by differentiation. These results comprehensively document that atRA and ddRA exert similar transcriptional changes in keratinocytes and also add new insights into the molecular mechanism influenced by retinoids in the epidermis. Furthermore, it suggests which ARCI patients could benefit from therapy with retinoids.
2014-08-01 | GSE58749 | GEO
Project description:Targets of Retinoic Acid (RA) and 3,4-didehydroretinoic acid (ddRA) were identified in primary human epidermal keratinocytes grown in the presence of atRA or ddRA for 4 and 24 hours. Retinoids (natural forms and synthetic derivatives of vitamin A) are used as therapeutic agents for numerous skin diseases such as keratinization disorders (e.g. ichthyoses) and psoriasis. Two endogenous ligands for retinoic acid receptors exist, retinoic acid (atRA) and 3,4-didehydroretinoic acid (ddRA). In primary human epidermal keratinocytes many transcriptional targets for atRA are known, whereas the targets for ddRA are unknown. In an attempt to determine the targets, we compared the effect of atRA and ddRA on transcriptional profiles in undifferentiated and differentiating human primary keratinocytes. First, as expected, many genes were induced or suppressed in response to keratinocyte differentiation. Furthermore, the two retinoids affected substantially more genes in differentiated keratinocytes (more than 350) than in proliferating keratinocytes (20). In differentiating keratinocytes markers of cornification were suppressed suggesting a de-differentiating effect by the two retinoids. When comparing the expression profile of atRA to that of ddRA, no differently regulated genes were found. The array analysis also found that a minor number of miRNAs and a large number of non-coding transcripts were changed during differentiation and in response to the two retinoids. Furthermore, the expression of all, except one, genes known to cause autosomal recessive congenital ichthyosis (ARCI) were found to be induced by differentiation. These results comprehensively document that atRA and ddRA exert similar transcriptional changes in keratinocytes and also add new insights into the molecular mechanism influenced by retinoids in the epidermis. Furthermore, it suggests which ARCI patients could benefit from therapy with retinoids. Proliferating and differentiated keratinocytes were harvested after 4 and 24 hours after treatment with atRA, ddRA and vehicle for RNA extraction and hybridization on Affymetrix microarrays. Triplicate samples were generated for each time point and each treatment.
2014-08-01 | E-GEOD-58749 | biostudies-arrayexpress
Project description:Genome-wide 10k SNP profiling of FOXM1B-transduced N/TERT and primary normal human epidermal keratinocytes (NHEK). The aim of this study was to study the cancer initiation role of UVB and FOXM1B upregulation in NHEK. Upregulation of FOXM1B alone (without UVB) was found to directly induce genomic instability in the form of copy number aberration (CNA) and low levels of loss of heterozygosity (LOH) in primary NHEK. The FOXM1B-induced CNA was found to be retained and accumulated in subsequent cell culture passages. UVB-exposure resulted in significant chromosomal LOH and CNA in N/TERT cells expressing FOXM1B but not in EGFP-expressing cells. This indicates that UVB corroborated with FOXM1B to recruit LOH and CNA which may predispose cell to malignant transformation. Collectively, these results indicate that aberrant upregulation of FOXM1B in skin keratinocytes following UVB exposure may be an early mechanism whereby cells acquire genomic changes required for oncogenesis. Keywords: Genome-wide SNP profiling for loss of heterozygosity (LOH) and copy number aberration (CNA), FOXM1, UVB, Keratinocytes, Basal cell carcinoma, genomic instability, carcinogenesis, squamous cell carcinoma. 1) Three individual normal primary NHEK cultures were retrovirally transduced (with either EGFP or EGFP-FOXM1B) and left to grow for 4 days prior to SNP array analysis. 2) EGFP or EGFP-FOXM1B-tansduced NHEK cells were harvested at passage 1, 2 and 3 for SNP array analysis to investigate if genomic instability is maintained and accumulated in subsequent passages. 3) N/TERT cells transduced with either EGFP or EFOX were UVB-irradiated and left to grow for 50 days in culture prior to SNP array analysis.
2010-07-29 | E-GEOD-16937 | biostudies-arrayexpress
Project description:Urocanic acid (UCA) is a major epidermal chromophore that undergoes trans to cis photoisomerisation following exposure to solar ultraviolet radiation (UVR). Although there is considerable evidence that cis-UCA suppresses cell-mediated immune response in mouse skin, the molecular events are not fully understood. In this study, we examined involvement of gene transcription in the immunomodulatory effects of cis-UCA on primary human keratinocytes. The results showed that about 400 genes were induced by UVR, 16 of which also up-regulated by cis-UCA. In contrast, trans-UCA had no effect on gene expression. The genes up-regulated by both cis-UCA and UVR were associated with apoptosis, cell growth arrest, cytokines and oxidative stress. Experiment Overall Design: RNA was extracted from primary human keratinocytes treated with trans-, cis-UCA (10ug/ml) or solar simulated UVR (12J/cm2 ~ 2-3 minimal erythema doses for fair skin), or untreated. At 24hr, the transcriptional profiles were assessed by Affymetrix HG-U133A microarray.
2008-11-06 | E-GEOD-8760 | biostudies-arrayexpress
Project description:Genome-wide 10k SNP profiling of FOXM1B-transduced N/TERT and primary normal human epidermal keratinocytes (NHEK). The aim of this study was to study the cancer initiation role of UVB and FOXM1B upregulation in NHEK. Upregulation of FOXM1B alone (without UVB) was found to directly induce genomic instability in the form of copy number aberration (CNA) and low levels of loss of heterozygosity (LOH) in primary NHEK. The FOXM1B-induced CNA was found to be retained and accumulated in subsequent cell culture passages. UVB-exposure resulted in significant chromosomal LOH and CNA in N/TERT cells expressing FOXM1B but not in EGFP-expressing cells. This indicates that UVB corroborated with FOXM1B to recruit LOH and CNA which may predispose cell to malignant transformation. Collectively, these results indicate that aberrant upregulation of FOXM1B in skin keratinocytes following UVB exposure may be an early mechanism whereby cells acquire genomic changes required for oncogenesis. Keywords: Genome-wide SNP profiling for loss of heterozygosity (LOH) and copy number aberration (CNA), FOXM1, UVB, Keratinocytes, Basal cell carcinoma, genomic instability, carcinogenesis, squamous cell carcinoma.
2010-06-28 | GSE16937 | GEO
Project description:To explore the biological changes of keratinocytes in condyloma acuminata (CA) warts, we performed mRNA and lncRNA expression profiling of keratinocytes from normal skins and warts of condyloma acuminata patients to compare the gene expression.
2020-03-11 | GSE140662 | GEO
Project description:Urocanic acid (UCA) is a major epidermal chromophore that undergoes trans to cis photoisomerisation following exposure to solar ultraviolet radiation (UVR). Although there is considerable evidence that cis-UCA suppresses cell-mediated immune response in mouse skin, the molecular events are not fully understood. In this study, we examined involvement of gene transcription in the immunomodulatory effects of cis-UCA on primary human keratinocytes. The results showed that about 400 genes were induced by UVR, 16 of which also up-regulated by cis-UCA. In contrast, trans-UCA had no effect on gene expression. The genes up-regulated by both cis-UCA and UVR were associated with apoptosis, cell growth arrest, cytokines and oxidative stress. Keywords: Agent response
2007-08-16 | GSE8760 | GEO
Project description:We applied digital RNA sequencing to explore the expression profiles of human epidermal keratinocytes carrying HPV 16E7.
2023-02-13 | GSE145224 | GEO
Project description:FGFs are key orchestrators of development, tissue homeostasis and repair. FGFR deficiency in mouse keratinocytes causes an inflammatory skin phenotype resembling atopic dermatitis (AD). To determine the human relevance of this finding, we generated human keratinocytes with a CRISPR/Cas9-induced knockout of FGFR2. Loss of this receptor promoted the expression of interferon-stimulated genes and other genes involved in inflammation under homeostatic conditions and in particular in response to inflammatory mediators without affecting cell viability. Bioinformatics analyses and functional studies showed strong down-regulation of FGFR2 expression in cultured keratinocytes exposed to various pro-inflammatory stimuli and in keratinocytes of lesional AD skin, which is likely to further aggravate the inflammatory phenotype. These results reveal a key function of FGFR2 in human keratinocytes in the suppression of skin inflammation and suggests a role of FGFR2 down-regulation in AD pathogenesis.
2024-08-29 | GSE267530 | GEO