MiRNAs expression in supernatant after ultraviolet irradiation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE111444 | GEO | 2018/03/07
REPOSITORIES: GEO
Similar Datasets
Project description:To test whether there is a photoprotective benefit after different types of suberythemal repetitive UV, a 1.5 MED challenge dose was applied 1 week after the initial 2 weeks of repetitive irradiation. To determine what different mechanisms and/or factors might be involved in physiological pigmentary responses of the skin to different types of UV, we used whole human genome microarrays and immunohistochemical analyses to characterize human skin in situ to examine how melanocyte-specific proteins and paracrine melanogenic factors are regulated by repetitive exposure to suberythemal doses of different types of UV (UVA and/or UVB). Seven volunteers with skin type II-III were irradiated with UVA, UVB or UVA+UVB radiation for 2 weeks (5 times per week, 10 times total) after preliminary determination of their MEDs. A UVA+UVB challenge dose of 1.5X the MED was applied 1 week later. Biopsies were taken before the challenge dose, immediately after the challenge dose, 4 days after the challenge, and 15 weeks after the challenge.
2014-12-12 | E-GEOD-56754 | biostudies-arrayexpress
Project description:We analysed the whole-genome transcriptional profile of 6 cell lines of dark melanocytes (DM) and 6 of light melanocytes (LM) at basal conditions and after UVB at different time points (6, 12 and 24h) to investigate the mechanisms by which melanocytes protect human skin from the damaging effects of ultraviolet-B radiation (UVB). Further, we assessed the effect of different keratinocyte-conditioned media (KCM+ and KCM-) on melanocytes. We analysed six lines of melanocytes isolated from lightly pigmented neonatal foreskin (LM), and six lines from darkly pigmented neonatal foreskin (DM), at 0, 6, 12 and 24 hours post UV irradiation. We also assessed the effect of different keratinocyte-conditioned media (KCM+ or KCM-)
2015-08-08 | E-GEOD-70280 | biostudies-arrayexpress
Project description:UVA1 makes up ~75% terrestrial ultraviolet radiation (UVR) is increasingly being used for the treatment for inflammatory skin disorders. It is also the major UVR spectral source in tanning lamps, however we lack human data to understand its effects on gene expression and further consequences. Using erythemally equivalent doses of UVA1 (50J/cm2) and UVB (30mJ/cm2) ~1MED (minimal erythema dose), this study examines time dependent whole genome expression, mRNA and protein changes in 12 skin types I/II individuals. The top upregulated pathway at 6h is inflammation through IL17 signaling for UVA1 (p=1.16e-6) and UVB (p=2.1e-4). At 24h the top upregulated pathway is extracellular matrix remodeling for UVA1 (p=5.5e-7) and UVB (p=2.9e-22). We show key spectral differences with matrix metalloproteinases (MMP): UVB upregulates MMP1 mRNA (p=0.0062), MMP3 mRNA (p=0.0016), MMP10 mRNA (p=0.028) at 24h compared to UVA1, MMP12 mRNA is upregulated by UVA1 at 6h and not by UVB (p=0.02). In a further 3 skin type I/II we show that MMP12 protein is formed by UVA1 (p=0.04) at 24h and that DQM-bM-^DM-" collagen type IV(likely MMP12 activity) hydrolysis occurs by UVA1 (p=0.027) at 10h. DQM-bM-^DM-" collagen type I hydrolysis occurs predominantly by UVB at 24h (p=0.031). Both UVA1 and UVB upregulate MMP1 at 10h and 24h. There is more MMP1 and MMP12 protein and activity in the epidermis than in dermis in all volunteers. We conclude that the biological processes that occur after 24h in human skin in vivo in response to erythemally equivalent doses of UVA1 and UVB are similar however there are key spectral differences: UVB plays a larger role in upregulating key MMPs in the epidermis. MMP12 is a UVA1 specific biomarker found predominantly in the epidermis and maybe useful as a marker of UVA1 exposure. We hypothesise that its formation by UVA1 could be related to the ability of UVA1 to produce significantly more oxidatively generated DNA than UVB (8oxodG). 47 samples were processed. The RNA was isolated from human skin samples of individual donors pre- or post irradiation with UVA or UVB. Skin biopsies were taken either before, 6h post, or 24h post exposure. Different doses of UVA were applied. Each condition was available from five or nine individuals, as indicated in the samples description below.
2014-05-15 | E-GEOD-45493 | biostudies-arrayexpress
Project description:To test the hypothesis that different mechanisms and/or factors might be involved in physiological pigmentary responses of the skin to different types of UV, we used whole human genome microarrays and immunohistochemical analyses to characterize human skin in situ to examine how melanocyte-specific proteins and paracrine melanogenic factors are regulated by repetitive exposure to suberythemal doses of different types of UV (UVA, UVB or SSR). Six volunteers with skin type II-III were irradiated with SSR, UVA or UVB radiation for 2 weeks (5 times per week, 10 times total) after preliminary determination of their MEDs. Biopsies were taken 3 days after the last irradiation.
2010-08-18 | E-GEOD-21429 | biostudies-arrayexpress
Project description:Despite widespread use of sunscreens that minimize erythema by blocking ultraviolet B (UVB) radiation, incidence rates of melanoma continue to rise. In considering this disparity between intervention and disease prevalence, we investigated the in vivo transcriptome of human skin treated with sunscreen and solar-simulated radiation (ssR). A focal skin area of healthy participants was exposed to ssR at 1 minimal erythema dose (MED), 0.1 MED or 100 J/m2 with or without prior application of sunscreen, or to non-UVB-spectrum of ssR (solar-simulated UVA/visible/infrared radiation: ssA). Skin biopsies were analyzed using expression microarrays.
2011-10-19 | GSE22083 | GEO
Project description:Kertinocyte cultures grown in 60 mm petri dishes were placed 186 mm from the solar simulator source (Solar-simulated ultraviolet radiation 1600W Xenon short arc lamp with an Oriel Air Mass 1 Direct Filter, (AM1:D:B; model 81074) and KG2 Short Pass Filter. irradiance 9.84 mW/cm² for UVA (98.3%), 0.174 mW/cm² for UVB (1.7%) and 10 mW/cm² (0.017 mW/cm² erythemally-weighted) for the total UVR irradiance) and received a dose of either 0, 10, 20 and 150 kJ/m2 of unweighted ultraviolet radiation and 0, 10 and 150 kJ/m2 of unweighted ultraviolet radiation with SPF 15 sunscreen filtration (Homosalate 3%, Octisalate 4%, Avobenzone 2%, Titanium dioxide 0.66%) (2 mg/cm2 sandwiched between two 5x5 inch quartz plates) and were temperature controlled at 37oC using a customized water-bath. Six and Twenty-four hours post-exposure cells were harvested and RNA was extracted and subjected to microarray analysis.
2018-09-07 | GSE103621 | GEO
Project description:Ultraviolet (UV) wavebands in sunlight are immunomodulatory. About half the amount of UVA within a minimum erythemal dose of sunlight is systemically immunosuppressive, while higher doses protect from UVB immunosuppression in mice. We have previously shown that these responses to UVA are genetically restricted as they occur in C57BL/6 but not Balb/c mice. We used gene set enrichment analysis of microarray data and real-time RT-PCR confirmation to determine the molecular mechanisms associated with UVA immunomodulation. We found up-regulation of mRNA for the alternative complement pathway. The core-enriched genes complement component 3, properdin and complement factor B were all activated by the immunosuppressive dose of UVA only in UVA-responsive C57BL/6 but not unresponsive BALB/c mice. This therefore matched the genetic restriction and dose responsiveness of UVA immunosuppression. The immune-protective higher UVA dose prevented UVB from down regulating chemokine receptor 7 and IL-12B, and decreased IL-10, supporting previous identification of IL-12 and IL-10 in high dose UVA protection from UVB immunosuppression. Our study has identified activation of the alternative complement pathway as a trigger of UVA-induced systemic immunosuppression and suggests that this pathway is likely to be an important sensor of UVA-induced damage to the skin. 24 hours after UVA, UVB and ssUV irradiation, a 1 cm2 uniform section of skin was excised from the dorsal surface of irradiated and control mice. Total RNA was then extracted from the whole skin using TRIzol reagent (Gibco Invitrogen Life Technologies, Carlsbad, CA, USA) according to the manufacturerâ??s instructions, purified, DNase treated and reverse transcribed into cDNA. For the microarray study a direct incorporation of Cyanine 3-dCTP and Cyanine 5-dCTP fluorescent dyes (Perkin Elmer Life Sciences, Inc. Boston, MA, USA) was used for cDNA synthesis. For each UV dose, a reference design was used to compare an unirradiated control against an irradiated sample. Microarray experiments used compugen 22k mouse oligonucleotide microarray slides (The Clive and Vera Ramaciotti Centre for Gene Function Analysis, Sydney Australia (http://www.ramaciotti.unsw.edu.au). Lower and higher UVA doses were used. C57BL/6 mice were irradiated with lower UVA, higher UVA, UVB, or ssUV; Balb/C mice were irradiated with lower or higher UVA. Experiments were replicated 6 times for each UV dose. A fluorescent dye swap was done for each alternate hybridisation to reduce systematic dye bias of incorporated fluorescent dyes.
2010-05-16 | E-GEOD-15618 | biostudies-arrayexpress
Project description:The UVB component of the sunlight (290-320 nm) plays an important role in carcinogenesis through generation of high levels of bipyrimidine DNA photoproducts, while UVA (320-400 nm) has been associated with photoaging and tumor progression through generation of low, but continuous levels of DNA damage and oxidative stress. However, the contribution of UVA light to epidermal cell fate in the context of photoaging remains poorly understood. Here, by using proteomic analyses and biochemical assays for validation, we show that UVA induces proteome remodeling and senescence in primary keratinocytes, eliciting potent antioxidant and pro-inflammatory responses. As a model of early skin tumorigenesis during aging, immortalized non-malignant keratinocytes, bearing potentially oncogenic mutations and dysfunctional components of the senescent machinery , are resilient to UVA-induced stress, but are sensitive to paracrine oxidative stress and immune system activation induced by senescent neighboring keratinocytes. These observations reveal a new cellular mechanism by which UVA induces photoaging in the epidermis.
2022-02-17 | PXD025191 | Pride
Project description:Skin cancer is the most prevalent cancer in humans, especially in the United States, Australia, and New Zealand. Australia and New Zealand are the two countries with the highest rates of skin cancer in the world, about four times higher than the United States, the United Kingdom and Canada. According to statistics, one American dies of skin cancer every hour. Studies have shown that ultraviolet radiation is the main cause of skin cancer, and ultraviolet rays are mainly divided into UVA, UVB and UVC according to wavelength, UVA and UVB can cause DNA damage, and UVB is the main factor that induces skin cancer. UVB is primarily a direct damage to cellular DNA and generally includes the formation of pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). UVB can also cause mutations in tumor suppressor genes such as p53, ptch, and ras. These bases the mutation will promote the activation of related signaling pathways, thereby inducing the production of tumors.In this study, we will use gene chip technology to screen out UVB-sensitive genes, and then select the genes of the UVB-sensitive GPCR family from these genes, and further use PCR for verification, so as to identify UVB-sensitive GPCRs, which will provide a basis for further experimental research.
2024-01-16 | GSE251673 | GEO
Project description:Background: Infrared A radiation (IRA 760-1440 nm) is a major component of solar radiation and, similar to ultraviolet (UV) radiation, causes photoaging of human skin by increasing the expression of matrixmetalloproteinase-1 (MMP-1) expression in human skin fibroblasts. This gene-regulatory effect resulted from the IRA induced activation of the pleiotropic MAPKinase ERK1/2 signaling pathway, indicating that the IRA response extends beyond MMP-1. In the present study we have therefore assessed the IRA-induced transcriptom in primary human skin fibroblasts. Results: Microarray analysis revealed 599 transcripts to be regulated by physiologically relevant doses of IRA in primary human skin fibroblasts. The IRA induced transcriptom differed from changes known to be induced by UVB or UVA radiation in the same cell type. IRA responsive genes include four categories: extracellular matrix, calcium homeostasis, stress signaling, and apoptosis. These results were confirmed by realtime PCR experiments analyzing thirteen of these genes representing these four categories. By means of chemical inhibitors of known signaling pathways we next show that besides ERK1/2, the p38-, JNK-, PI3K/AKT-, STAT3-, and IL-6 as well as calcium mediated signaling pathways are functionally involved in the IRA gene response and that a major part of it is triggered by mitochondrial, and to a lesser extent non-mitochondrial production of reactive oxygen species. Conclusion: This study identifies IRA radiation as a potent modulator of gene expression in human skin cells. The IRA response is specific and involves genes which are of critical importance for the homeostasis of human skin. Our data confirm the previous notion that IRA contributes to premature skin aging and indicate that further biological effects may result from IRA exposure of human skin. To identify genes differentially regulated after IRA irradiation we analyzed a set of nine independent samples pairs (IRA irradiated vs. sham irradiated), using human primary human dermal fibroblasts from three different donors (termed F1 to F3). Cells between passage number five to ten were exposed in vitro to a dose of 860 J/cm2 IRA. IRA irradiation lasted 40 min leading to a total dose of 860 J/cm2. The culture dishes were placed on a cooled plate connected to thermostated bath (Thermo Haake GmbH, Karlsruhe, Germany) to maintain temperatures below 37°C during IRA irradiation. For irradiation, medium was replaced by phosphate-buffered saline (37°C, Gibco). Control cells (sham) were held on a 37°C thermostated plate under similar conditions without irradiation. Following the treatment cells were cultivated for 24 hours with serum free MEM culture medium at 37°C.
2010-07-10 | E-GEOD-17046 | biostudies-arrayexpress