Modulatory role of skin microbiome against UV
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA481877 | ENA |
REPOSITORIES: ENA
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Project description:The role of the skin microbiome in UV-induced immune suppression has been overlooked. We addressed the question of microbial involvement in UV-induced immune suppression by using the standard model of contact hypersensitivity in the presence or absence of the microbiome (in germ-free [GF] and disinfected mice) and found that the microbiome inhibits UV-induced immune suppression. Furthermore, our transcriptome analysis (24 hours after irradiation) showed differential regulation of many genes in the presence or absence of the microbiome, including a predominance of pro-inflammatory cytokines versus immunosuppressive cytokines
2019-05-26 | GSE117359 | GEO
Project description:Tanning is a skin protection mechanism against UV radiation. Pigment production initiates hours after exposure, and the mechanism controlling this delay was unknown. Here we reveal a skin UV-protection timer, governed by damped oscillatory dynamics of the melanocyte master regulator, MITF, which after UV exposure, synchronizes regulatory programs, first cell survival and later pigmentation. Remarkably, the same amount of UV dosage resulted in higher pigmentation of human skin when given every-other day compared to daily exposure. Daily UV exposure appears to perturb MITF dynamics, thus re-ordering the survival and pigmentation programs. This demonstrates that the skin is more sensitive to frequency than quantity of UV exposure. Mathematical modeling identified a double negative regulatory loop involving HIF1a and microRNA-148a that regulates MITF dynamics. Our study suggests evolutionary leverage of the UV-protection timer, as it evolved to induce maximum protection with minimum damage for the reduction of skin cancer risk.
2018-10-26 | GSE114764 | GEO
Project description:Epigenetic alterations are a driving force of the carcinogenesis process. MicroRNAs play a role in silencing mutated oncogenes, thus defending the cell against the adverse consequences of genotoxic damages induced by environmental pollutants. These processes have been well investigated in lungs; however, although skin is directly exposed to a great variety of environmental pollutants, more research is needed to better understand the effect on cutaneous tissue. Therefore, we investigated microRNA alteration in human skin biopsies exposed to diesel fumes, ozone, and UV light for over 24 h of exposure. UV and ozone-induced microRNA alteration right after exposure, while the peak of their deregulations induced by diesel fumes was reached only at the end of the 24 h. Diesel fumes mainly altered microRNAs involved in the carcinogenesis process, ozone in apoptosis, and UV in DNA repair. Accordingly, each tested pollutant induced a specific pattern of microRNA alteration in skin related to the intrinsic mechanisms activated by the specific pollutant. These alterations, over a short time basis, reflect adaptive events aimed at defending the tissue against damages. Conversely, whenever environmental exposure lasts for a long time, the irreversible alteration of the microRNA machinery results in epigenetic damage contributing to the pathogenesis of inflammation, dysplasia, and cancer induced by environmental pollutants.
2022-03-11 | GSE198333 | GEO
Project description:Solar UV represents a ubiquitous environmental physical insult. Thus, to maintain its integrity as an effective barrier, skin must be unusually resistant to cell death. However, UV overexposure causes sunburn1,2 (necrosis and inflammation) and cells that survive harbour damaged DNA, which if not repaired or removed by apoptosis can lead to skin cancer development3-10. CD1d, a transmembrane protein identified in glycolipid antigen presentation11,12 to invariant natural killer T (NKT) cells13,14 is expressed by epithelial cells of most tissues including skin15-17, and shares close homology between humans and mice12. Since CD1d and NKT cells are implicated in regulating UV skin carcinogenesis4,18, we studied susceptibility to UV-induced sunburn in mice either lacking expression of both CD1d and NKT cells or expressing CD1d without NKT cells. Here we show that CD1d, but not NKT cells is necessary for UV to cause sunburn. CD1d causes cells to resist apoptosis in response to UV overexposure as the means to promote cell survival and directs the expression of inflammatory response genes, resulting in tissue destruction and skin inflammation. This previously unknown action of CD1d links the etiology of sunburn to skin cancer. Keywords = CD1d knockout, UV, sunburn, cancer Keywords: other
2016-11-27 | GSE2436 | GEO
Project description:We conducted transcript profiling and metabolome profiling induced by UV irradiation in grape berry skin. Transcriptome analysis was carried out with genome-wide microarray and two hundred thirty eight genes were more than 5-fold up-regulated by UV irradiation. The enrichment analysis showed GO terms including stilbene synthase (STS) gene. Moreover, the principal component analysis (PCA) of metabolome analysis showed a compound, identified resveratrol, accumulated in grape berry skin specifically. Our result clearly shows that UV irradiation induced only accumulation of resveratrol and its analogues but did not induce accumulation of the other phenolic compounds.
2014-12-01 | GSE59436 | GEO
Project description: Not available
| S-EPMC7369546 | biostudies-literature
Project description:Although excessive exposure to UV is widely recognized as a major factor leading to skin perturbations and cancer, the complex mechanisms underlying inflammatory skin disorders resulting from UV exposure remain incompletely characterized. The nuclear hormone receptor PPARβ/δ is known to control cutaneous repair and UV-induced cancer development. Here, we describe a novel PPARβ/δ-dependent molecular cascade involving TGFβ-1 and miR-21-3p, which is activated in the epidermis in response to UV exposure. We establish that the passenger miRNA miR-21-3p, that we identify as a novel UV-induced miRNA in the epidermis, plays a pro-inflammatory function in keratinocytes, and that its high level of expression in human skin is associated with psoriasis and squamous cell carcinomas. Finally, we provide evidence that inhibition of miR-21-3p reduces UV-induced cutaneous inflammation in ex vivo human skin biopsies, thereby underlining the clinical relevance of miRNA-based topical therapies for cutaneous disorders.
2016-06-03 | GSE80428 | GEO
Project description:Although excessive exposure to UV is widely recognized as a major factor leading to skin perturbations and cancer, the complex mechanisms underlying inflammatory skin disorders resulting from UV exposure remain incompletely characterized. The nuclear hormone receptor PPARβ/δ is known to control cutaneous repair and UV-induced cancer development. Here, we describe a novel PPARβ/δ-dependent molecular cascade involving TGFβ-1 and miR-21-3p, which is activated in the epidermis in response to UV exposure. We establish that the passenger miRNA miR-21-3p, that we identify as a novel UV-induced miRNA in the epidermis, plays a pro-inflammatory function in keratinocytes, and that its high level of expression in human skin is associated with psoriasis and squamous cell carcinomas. Finally, we provide evidence that inhibition of miR-21-3p reduces UV-induced cutaneous inflammation in ex vivo human skin biopsies, thereby underlining the clinical relevance of miRNA-based topical therapies for cutaneous disorders.
2016-06-03 | GSE80429 | GEO
Project description:Although excessive exposure to UV is widely recognized as a major factor leading to skin perturbations and cancer, the complex mechanisms underlying inflammatory skin disorders resulting from UV exposure remain incompletely characterized. The nuclear hormone receptor PPARβ/δ is known to control cutaneous repair and UV-induced cancer development. Here, we describe a novel PPARβ/δ-dependent molecular cascade involving TGFβ-1 and miR-21-3p, which is activated in the epidermis in response to UV exposure. We establish that the passenger miRNA miR-21-3p, that we identify as a novel UV-induced miRNA in the epidermis, plays a pro-inflammatory function in keratinocytes, and that its high level of expression in human skin is associated with psoriasis and squamous cell carcinomas. Finally, we provide evidence that inhibition of miR-21-3p reduces UV-induced cutaneous inflammation in ex vivo human skin biopsies, thereby underlining the clinical relevance of miRNA-based topical therapies for cutaneous disorders.
2016-06-03 | GSE80427 | GEO
Project description:Pseudomonas aeruginosa treated with UV against untreated controls
| PRJEB40577 | ENA