UVB Irradiation Differential Regulate miRNAs Expression in Acute Skin Injury
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ABSTRACT:
PROVIDER: PRJNA752884 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15369400.fastq.gz | Fastqsanger.gz | |||
| SRR15369401.fastq.gz | Fastqsanger.gz | |||
| SRR15369402.fastq.gz | Fastqsanger.gz | |||
| SRR15369403.fastq.gz | Fastqsanger.gz | |||
| SRR15369404.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: to explore the function and mechanism of skin damage induced by ultraviolet irradiation. The mouse model of UVB irradiation was established. Using miRNA Sequence analysis, the miRNA expression profile of the mouse skin model exposed to UVB radiation and the normal skin mice. GO and Pathway analysis were employed for the prediction of miRNA targets. Results:Compared with normal skin, a total of 23 miRNAs were screened for significantly different expressions. Among them, 7 miRNAs were up-regulated and 16 were down-regulated in the skin wound tissue of mice exposed to UVB irradiation. The differential expression of miRNA is related to a variety of signal transduction pathways, among which mmu-miR-195a-5p and mitogen-activated protein kinase (MAPK) signal pathway is worthy of attention. Conclusion: There was significant difference expression of miRNA in the skin tissue of normal mice and the skin injury induced by UVB irradiation. Differential expression of miRNA can be used in the diagnosis and treatment of UVB-induced acute skin injury.
2024-08-08 | GSE181657 | GEO
Project description:BackgroundUVB irradiation can cause acute damage such as sunburn, or photoaging and melanoma, all of which are major health threats.ObjectiveThis study was designed to investigate the mechanism of skin photoaging induced by UVB radiation in mice through the analysis of the differential expression of miRNAs.MethodsA UVB irradiation photoaging model was constructed. HE and Masson special stains were used to examine the modifications in the epidermis and dermis of mice. The miRNA expression profiles of the mouse skin model exposed to UVB radiation and the normal skin of mice were analyzed using miRNA-sequence analysis. GO and Pathway analysis were employed for the prediction of miRNA targets.ResultsA total of 23 miRNAs were evaluated for significantly different expressions in comparison to normal skin. Among them, 7 miRNAs were up-regulated and 16 were down-regulated in the skin with photoaging of mice exposed to UVB irradiation. The differential expression of miRNA is related to a variety of signal transduction pathways, among which mmu-miR-195a-5p and mitogen-activated protein kinase (MAPK) signal pathways are crucial. There was a significant differential expression of miRNA in the skin of normal mice in comparison with the skin with photoaging induced by UVB irradiation.Study limitationsDue to time and energy constraints, the specific protein level verification, MAPK pathway exploration, and miR-195a-5p downstream molecular mechanism need to be further studied in the future.ConclusionsUVB-induced skin photoaging can be diagnosed and treated using miRNA.
| S-EPMC9263642 | biostudies-literature
Project description:Analysis of gene expression in mouse lens epithelium with or without UVB-irradiation in mouse eye lens. Results provide insight into a role for the respons to UVB-irradiation in lens epithelial cells.
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Project description:In response to ultraviolet radiation (UVR), cells alter gene expression, switching on a variety of damage response pathways. Long non-coding RNA (lncRNA) is thought to play critical roles in regulating expression of protein-coding genes. We hypothesized that lncRNAs also regulate gene expression following UV exposure and screened for changes in lncRNA expression in human primary fibroblasts after irradiation with longwave UV (UVA) or shortwave UV (UVB).
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Project description:Dr. Liu's research group is interested in studying the expression and functions of galectin-3, -7 and -12, in particular the roles of these proteins in inflammation and neoplasm. Members of the galectin family are known to participate in cellular homeostasis by modulating cell growth, controlling cell cycle progression, and inducing or inhibiting apoptosis. It is known that some galectins have similar functions. However, it is not fully understood whether they work cooperatively or not. As the outermost barrier of the body, skin is directly and frequently exposed to a prooxidative environment, including solar ultraviolet A (UVA), ultraviolet B (UVB) radiation, and air pollution. Several reports have shown that exposure of cells to UV increase or decrease the levels of galectins. For example, the amounts of galectin-7 mRNA and protein are increased rapidly after UVB irradiation of keratinocytes (Proc. Natl. Acad. Sci. USA 1999; 96:11329-34). Heat shock and subculturing decrease, while alkylating agents and UV-light increase galectin-3 (Cell Physiol Biochem 2000; 10:149-58). To analyze the change of all galectin gene expression profiles after UVB irradiation and to determine the presence or absence of coordinate regulation, we analyzed the gene expression profiles of keratinocytes exposed to UVB. Normal human epidermal keratinocytes (NHEK) were irradiated with 200 J/m2 of UVB. Total RNA will be extracted at 0, 6, 12 and 24 h after irradiation (duplicate) for analysis on the Glyco gene chip. Several reports have shown that exposure to UV light can regulate levels of galectin in skin. This study seeks to analyze the changes in all galectin gene expression profiles post-UVB irradiation to determine the presence or absence of coordinate regulation. In this study, normal human keratinocytes were irradiated with 200J/m2 of UVB. Total RNA was extracted at 0, 6, 12, and 24-hour post irradiation time points, in duplicate. Samples were hybridized and analyzed using the GLYCOv2 array.
2011-02-17 | E-GEOD-27360 | biostudies-arrayexpress
Project description:Renin-angiotensin system regulates cell proliferation, differentiation, apoptosis and tissue remodeling in skin. Previouly, we reported that angiotensin-converting enzyme (ACE) expression and angiotensin II level were enhanced by repeated UVB-irradiation of hairless mice skin, and ACE inhibitor enalapril maleate accelerated recovery of UVB-induced wrinkle. In present study, we analyzed gene expression with DNA microarray and protein distribution with immunofluorecence method to clarify the process of wrinkle repairing with enalapril maleate in UVB-irradiated hairless mouse. In microarray analysis, we detected up-regulation of various extracullular matrix (ECM) genes and ECM related genes. In immunofluorescence, we confirm that type 1 collagen, fibrillin1, elastin, and dystroglycan 1 were decreased by repeated UVB-irradiation and the distribution of these components were improved by enalapril maleate treatment. In addition, ADAMTS2 and MMP-14, these were perticipate in ECM structure formation and degradation, were increased in enalapril maleate-treated mouse skin. While the functions of these molecules in skin is not clear yet, it is suggested that these molecules participate in improvement of wrinkles induced by UVB-irradiation. SUBMITTER_CITATION: Yuko Matsuura-Hachiya, Yuji Nakai, Keiko Abe, Toshio Nishiyama, Koji Y. Arai (2015) "Recovery of extracellular matrix components by enalapril maleate during the repair process of ultraviolet B-induced wrinkles in mouse skin", Biochemistry and Biophysics Reports 4, 180-186, doi:10.1016/j.bbrep.2015.09.012
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Project description:To investigate the mechanism of radiation induced bystander effect, we explored miRNAs expression in supernatant of human skin fibroblasts after culturing for 24h post UV irradiation. Primary human skin fibroblasts were obtained from healthy volunteers by means of a foreskin circumcision. Human skin fibroblasts was irradiated with 20J/cm2 UVA or 60mJ/cm2 UVB. Expression of miRNAs were tested by microarray between radiation and control samples.
2018-03-07 | GSE111444 | GEO
Project description:Renin-angiotensin system regulates cell proliferation, differentiation, apoptosis and tissue remodeling in skin. Previouly, we reported that angiotensin-converting enzyme (ACE) expression and angiotensin II level were enhanced by repeated UVB-irradiation of hairless mice skin, and ACE inhibitor enalapril maleate accelerated recovery of UVB-induced wrinkle. In present study, we analyzed gene expression with DNA microarray and protein distribution with immunofluorecence method to clarify the process of wrinkle repairing with enalapril maleate in UVB-irradiated hairless mouse. In microarray analysis, we detected up-regulation of various extracullular matrix (ECM) genes and ECM related genes. In immunofluorescence, we confirm that type 1 collagen, fibrillin1, elastin, and dystroglycan 1 were decreased by repeated UVB-irradiation and the distribution of these components were improved by enalapril maleate treatment. In addition, ADAMTS2 and MMP-14, these were perticipate in ECM structure formation and degradation, were increased in enalapril maleate-treated mouse skin. While the functions of these molecules in skin is not clear yet, it is suggested that these molecules participate in improvement of wrinkles induced by UVB-irradiation. Male hairless mice of the SKH-1 strain were purchased from Charles River Laboratories Japan, Inc. (Tokyo, Japan). These animals were approximately 6 weeks old at the start of the experiment. They were fed a commercial diet (CRF-1, Oriental Yeast Co., Ltd, Tokyo, Japan) ad libitum and allowed free access to water. The dorsal region of the mouse was repeatedly irradiated with UVB for 10 weeks. Enalapril maleate treatment was started at 1 week after 10-week irradiation. One hundred microliters of 1% w/v enalapril maleate dissolved in 30 vol % ethanol solution or 30 vol % ethanol (control) was applied 5 times a week for 2 consecutive weeks to the whole dorsal skin of each of the mice. All experimental procedures using mice were approved by the Animal Experiment Committee of Tokyo University of Agriculture and Technology (approval number 24-82). The dosal region of the mouse was repeatedly irradiated with UVB for 10 weeks. Enalapril maleate treatment was started at 1 week after 10-week irradiation. One hundred microliters of 1% w/v enalapril maleate dissolved in 30 vol % ethanol solution or 30 vol % ethanol (control) was applied 5 times a week for 2 or 6 consecutive weeks to the whole dorsal skin of each of the mice. Each of the experimental groups comprised 6 mice. After 2- or 6-week drug treatment, skin samples were collected for microarray analysis.
2015-09-24 | E-GEOD-61708 | biostudies-arrayexpress
Project description:UVB irradiation effect on mouse lens epithelium
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Project description:Dr. Liu's research group is interested in studying the expression and functions of galectin-3, -7 and -12, in particular the roles of these proteins in inflammation and neoplasm. Members of the galectin family are known to participate in cellular homeostasis by modulating cell growth, controlling cell cycle progression, and inducing or inhibiting apoptosis. It is known that some galectins have similar functions. However, it is not fully understood whether they work cooperatively or not. As the outermost barrier of the body, skin is directly and frequently exposed to a prooxidative environment, including solar ultraviolet A (UVA), ultraviolet B (UVB) radiation, and air pollution. Several reports have shown that exposure of cells to UV increase or decrease the levels of galectins. For example, the amounts of galectin-7 mRNA and protein are increased rapidly after UVB irradiation of keratinocytes (Proc. Natl. Acad. Sci. USA 1999; 96:11329-34). Heat shock and subculturing decrease, while alkylating agents and UV-light increase galectin-3 (Cell Physiol Biochem 2000; 10:149-58). To analyze the change of all galectin gene expression profiles after UVB irradiation and to determine the presence or absence of coordinate regulation, we analyzed the gene expression profiles of keratinocytes exposed to UVB. Normal human epidermal keratinocytes (NHEK) were irradiated with 200 J/m2 of UVB. Total RNA will be extracted at 0, 6, 12 and 24 h after irradiation (duplicate) for analysis on the Glyco gene chip.
2011-02-17 | GSE27360 | GEO