Transcriptome analysis identifies the dysregulation of ultraviolet target genes in human skin cancers
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE85443 | GEO | 2018/12/01
REPOSITORIES: GEO
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Project description:Skin damage from solar ultraviolet radiation (UVR) accumulates in the dermal extracellular matrix (ECM) and contributes to photoaging. Following UVR exposure, matrix metalloproteinases (MMPs) are secreted by dermal fibroblasts to repair and remodel the ECM. Molecular signaling pathways delineating the induction of MMPs are currently well-defined; however, the effects of UV exposure on epigenetic mechanisms of MMP induction are not as well understood. An epigenetic mechanism would further describe how MMP genes are regulated in response to UV. In this study, we examined solar simulated UVR (ssUVR)-induced gene expression changes and alterations to histone methylation in the promoters of MMP1 and MMP3 in primary human dermal fibroblasts (HDF). This set of gene expression data was generated to identify photoaging related genes (including MMP) that were impacted by ssUVR exposure in our system.
2014-08-27 | GSE60794 | GEO
Project description:Skin damage from solar ultraviolet radiation (UVR) accumulates in the dermal extracellular matrix (ECM) and contributes to photoaging. Following UVR exposure, matrix metalloproteinases (MMPs) are secreted by dermal fibroblasts to repair and remodel the ECM. Molecular signaling pathways delineating the induction of MMPs are currently well-defined; however, the effects of UV exposure on epigenetic mechanisms of MMP induction are not as well understood. An epigenetic mechanism would further describe how MMP genes are regulated in response to UV. In this study, we examined solar simulated UVR (ssUVR)-induced gene expression changes and alterations to histone methylation in the promoters of MMP1 and MMP3 in primary human dermal fibroblasts (HDF). This set of gene expression data was generated to identify photoaging related genes (including MMP) that were impacted by ssUVR exposure in our system.
2014-08-27 | GSE60795 | GEO
Project description:Chronic, low-dose UV irradiation (UVR) leads to premature ageing of the skin characterised by wrinkles and loss of elasticity. Although the aged appearance of photoexposed skin may take years to manifest, the biochemical and molecular damage that underpins photoageing can occur following a single physiological dose of UVR. Understanding the damage mechanisms that are elicited in skin following acute UVR could help to inform strategies to delay photoageing. Targeted approaches show that UVR alters the abundance and structure of selected ECM proteins and protein assemblies, and these processes are driven by UV-induced reactive oxygen species (ROS). However, due to limitations in proteomic analysis, it has been difficult to evaluate the effects of acute UVR on an entire ECM-enriched proteome, containing hundreds of proteins. Peptide location fingerprinting (PLF) is a proteomic analysis tool that can identify structural changes in hundreds of proteins across different treatment groups using a non-targeted approach. The aim of this study was to use PLF to identify proteins within an ECM-enriched proteome that is structurally altered in response to UV. To
confirm the utility of PLF, structural changes in native type-I collagen, known to be UV-resistant, and purified human fibronectin, known to be UV susceptible, were evaluated following UVR at 50 mJ/cm2 and 500 mJ/cm2. Results show that native type-I collagen displays no significant structural changes in response to UVR, whereas UV irradiated human tissue fibronectin shows significant structural changes within the functional domains binding fibrin/heparin and collagen. Using a ECM-enriched proteome in vitro, PLF identifies 25 proteins from amongst a proteome of 977 proteins that show structural changes in response to acute UVR (100 mJ/cm2). The highly variable UV chromophore content among this group of 25 proteins suggests that abundance of UV chromophores alone cannot account for the structural changes observed in response to UVR. Protein interaction analysis (STRING) shows that UV targeted proteins are involved in collagen fibril formation, glycosaminoglycan metabolism and protein translation, and assessment of protein domain organization (Uniprot) shows that acute UV alters domains involved in ECM binding (COL5A1, versican) and myosin motility. In conclusion, this study identifies a select group of extracellular and intracellular dermal proteins that are susceptible to acute UVR and identifies the specific protein domains in which acute UV-mediated damage occurs.
2024-11-14 | PXD046907 | JPOST Repository
Project description:Skin damage from solar ultraviolet radiation (UVR) accumulates in the dermal extracellular matrix (ECM) and contributes to photoaging. Following UVR exposure, matrix metalloproteinases (MMPs) are secreted by dermal fibroblasts to repair and remodel the ECM. Molecular signaling pathways delineating the induction of MMPs are currently well-defined; however, the effects of UV exposure on epigenetic mechanisms of MMP induction are not as well understood. An epigenetic mechanism would further describe how MMP genes are regulated in response to UV. In this study, we examined solar simulated UVR (ssUVR)-induced gene expression changes and alterations to histone methylation in the promoters of MMP1 and MMP3 in primary human dermal fibroblasts (HDF). This set of gene expression data was generated to identify photoaging related genes (including MMP) that were impacted by ssUVR exposure in our system. Primary neonatal human dermal fibroblasts (HDF) were irradiated a single time with 12 J/cm2 ssUVR. The sham treatments are negative controls (0 J/cm2 ssUVR). The cells were collected for gene expression analysis 1 day after exposure, and then 5 days after exposure. Affymetrix GeneChip Human Exon 1.0 ST arrays were used to characterize gene expression pattern alterations in response to ssUVR.
2014-08-27 | E-GEOD-60795 | biostudies-arrayexpress
Project description:Skin damage from solar ultraviolet radiation (UVR) accumulates in the dermal extracellular matrix (ECM) and contributes to photoaging. Following UVR exposure, matrix metalloproteinases (MMPs) are secreted by dermal fibroblasts to repair and remodel the ECM. Molecular signaling pathways delineating the induction of MMPs are currently well-defined; however, the effects of UV exposure on epigenetic mechanisms of MMP induction are not as well understood. An epigenetic mechanism would further describe how MMP genes are regulated in response to UV. In this study, we examined solar simulated UVR (ssUVR)-induced gene expression changes and alterations to histone methylation in the promoters of MMP1 and MMP3 in primary human dermal fibroblasts (HDF). This set of gene expression data was generated to identify photoaging related genes (including MMP) that were impacted by ssUVR exposure in our system. Primary neonatal human dermal fibroblasts (HDF) were irradiated a single time with 0, 4, or 12 J/cm2 ssUVR. The sham treatments are negative controls (0 J/cm2 ssUVR). The cells were collected for gene expression analysis 24 hours after exposure. Affymetrix GeneChip Human Exon 1.0 ST arrays were used to characterize gene expression pattern alterations in response to ssUVR.
2014-08-27 | E-GEOD-60794 | biostudies-arrayexpress
Project description:UV radiation (UV) alters secondary metabolism in the skin of Vitis vinifera L. berries, which may affect on the final composition of both, grapes and wines. We compared berry skin transcriptome and phenolic composition between Tempranillo berries grown in the presence or absence of solar UV in a mid-altitude Tempranillo vineyard. By analysing two different ripening degrees, expression of 121 genes was significantly altered. Functional enrichment identified that, principally, secondary metabolism-related transcripts were induced by UV, including VvFLS1, VvGT5 and VvGT6 flavonol biosynthetic genes induction. Concurrently, flavonol accumulation was the most evident impact of UV on the berry skin phenolic composition. Monoterpenoid biosynthetic transcripts were also up-regulated by UV, whereas induction of stilbenoid biosynthetic transcripts and stilbenes accumulation was probably induced by the joint action of UV and other condition under the UV-blocking filter, likely higher temperature. Among regulatory genes, VvMYBF1, VvMYB24 and three bHLH transcription factors were up-regulated by UV. Homologs to Arabidopsis UVR8-dependent UV-B-induced genes were also induced, including VvHY5-1, VvHY5-2 and VvRUP UV-B signalling genes. This suggests that the UV-B-specific signalling pathway is activated in the skin of grapes grown at low-medium altitudes. The biosynthesis and accumulation of UV-absorbing compounds that are appreciated for winemaking were almost specifically triggered, which indicates that viticultural practices increasing solar UV incidence may improve grape features important to wine production.
2014-09-09 | GSE54636 | GEO
Project description:UV radiation (UV) alters secondary metabolism in the skin of Vitis vinifera L. berries, which may affect on the final composition of both, grapes and wines. We compared berry skin transcriptome and phenolic composition between Tempranillo berries grown in the presence or absence of solar UV in a mid-altitude Tempranillo vineyard. By analysing two different ripening degrees, expression of 121 genes was significantly altered. Functional enrichment identified that, principally, secondary metabolism-related transcripts were induced by UV, including VvFLS1, VvGT5 and VvGT6 flavonol biosynthetic genes induction. Concurrently, flavonol accumulation was the most evident impact of UV on the berry skin phenolic composition. Monoterpenoid biosynthetic transcripts were also up-regulated by UV, whereas induction of stilbenoid biosynthetic transcripts and stilbenes accumulation was probably induced by the joint action of UV and other condition under the UV-blocking filter, likely higher temperature. Among regulatory genes, VvMYBF1, VvMYB24 and three bHLH transcription factors were up-regulated by UV. Homologs to Arabidopsis UVR8-dependent UV-B-induced genes were also induced, including VvHY5-1, VvHY5-2 and VvRUP UV-B signalling genes. This suggests that the UV-B-specific signalling pathway is activated in the skin of grapes grown at low-medium altitudes. The biosynthesis and accumulation of UV-absorbing compounds that are appreciated for winemaking were almost specifically triggered, which indicates that viticultural practices increasing solar UV incidence may improve grape features important to wine production. A total of 12 samples were hybridized. Grape skin RNA from berries ripening under a UV-transmitting filter (FUV+) and a UV-blocking filter (FUV-) was compared. Berry skin of two different ripening stages was analysed on each UV treatment. All samples were harvested simultaneously and a NaCl series was used to select the ripening degree in a non-invasive way. Three biological replicates were analyzed for each sample.
2014-09-09 | E-GEOD-54636 | biostudies-arrayexpress
Project description:Exposure to ultraviolet (UV) irradiation is the major cause of nonmelanoma skin cancer, the most common form of cancer in the United States. UV irradiation has a variety of effects on the skin associated with carcinogenesis, including DNA damage and effects on signal transduction. The alterations in signaling caused by UV regulate inflammation, cell proliferation, and apoptosis. UV also activates the orphan receptor tyrosine kinase and proto-oncogene Erbb2 (HER2/neu). In this study, we demonstrate that the UV-induced activation of Erbb2 regulates the response of the skin to UV. Inhibition or knockdown of Erbb2 before UV irradiation suppressed cell proliferation, cell survival, and inflammation after UV. In addition, Erbb2 was necessary for the UV-induced expression of numerous proinflammatory genes that are regulated by the transcription factors nuclear factor-kappaB and Comp1, including interleukin-1beta, prostaglandin-endoperoxidase synthase 2 (Cyclooxygenase-2), and multiple chemokines. These results reveal the influence of Erbb2 on the UV response and suggest a role for Erbb2 in UV-induced pathologies such as skin cancer. Keywords: time course, ultraviolet irradiation, UV, erbB2, mouse skin
2006-07-01 | GSE4066 | GEO
Project description:Exposure to ultraviolet (UV) irradiation is the major cause of nonmelanoma skin cancer, the most common form of cancer in the United States. UV irradiation has a variety of effects on the skin associated with carcinogenesis, including DNA damage and effects on signal transduction. The alterations in signaling caused by UV regulate inflammation, cell proliferation, and apoptosis. UV also activates the orphan receptor tyrosine kinase and proto-oncogene Erbb2 (HER2/neu). In this study, we demonstrate that the UV-induced activation of Erbb2 regulates the response of the skin to UV. Inhibition or knockdown of Erbb2 before UV irradiation suppressed cell proliferation, cell survival, and inflammation after UV. In addition, Erbb2 was necessary for the UV-induced expression of numerous proinflammatory genes that are regulated by the transcription factors nuclear factor-kappaB and Comp1, including interleukin-1beta, prostaglandin-endoperoxidase synthase 2 (Cyclooxygenase-2), and multiple chemokines. These results reveal the influence of Erbb2 on the UV response and suggest a role for Erbb2 in UV-induced pathologies such as skin cancer. Keywords: time course, ultraviolet irradiation, UV, erbB2, mouse skin The dorsal skin of adult female CD-1 mice was clipped one day before treatment and shaved on the day of treatment. DMSO or 4 mg AG825 dissolved in DMSO was applied topically to the shaved back of the mice 2 h prior to exposure to 10 kJ/m^2 UV or sham irradiation. The UV dose was approximately 30% UVA, 70% UVB and <1% UVC, with a total output of 470 uW/cm^2. Flash frozen skin was removed and total RNA expracted with TRIzol reagent (Invitrogen) and further purified with an RNeasy kit (Qiagen). Amplification, reverse-transcription, biotinylation, and hybridization were all carried out under standard conditions and procedures recommended by the manufacturer.
2006-07-01 | E-GEOD-4066 | biostudies-arrayexpress
Project description:Scleractinian corals are the major builders of the complex structural framework of coral reefs. They live in tropical waters around the globe where they are frequently exposed to potentially harmful ultraviolet radiation (UVR). Coral eggs and early embryonic stages are thought to be the most sensitive life stages of corals to UVR given that they are highly buoyant and remain near the sea surface for prolonged periods of time. Here we analyzed gene expression changes in different larval stages of the Caribbean coral Montastraea faveolata to natural levels of UVR using high-density cDNA microarrays (10,930 clones). We found that larvae exhibit low sensitivity to natural levels of UVR during most time points analyzed as reflected by comparatively few transcriptomic changes in response to UVR. However, we identified a time window of high UVR sensitivity that coincides with the motile planula stage and the onset of larval competence. These processes have been shown to be affected upon UVR exposure, and the transcriptional changes we identified explain these observations well. Our analysis of differentially expressed genes indicates that UVR induces a stress response and affects the expression of neurogenesis-related genes that can be linked to swimming and settlement behavior at later stages. Taken together, our study provides further data to the impact of natural levels of UVR on coral larvae. Furthermore, our results might allow a better prediction of settlement and recruitment rates after coral spawning events based on UVR climate data.
2011-05-15 | GSE24949 | GEO