P38a-dependent gene expression in keratinocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE51206 | GEO | 2014/01/01
SECONDARY ACCESSION(S): PRJNA221593
REPOSITORIES: GEO
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Project description:Gene expression in wild-type and p38a-knockout keratinocytes were compared. Keratinocytes were isolated from newborn mice, and left unirradiated (0 h) and irradiated (4 h) with ultraviolet-B (UVB). C57BL/6 wild-type mice, and keratinocyte-specific p38a-knockout mice on a C57BL/6 background were used for isolation of primary keratinocytes. Gene expression in keratinocytes was analyzed 0 and 4 h after UVB irradiation (75 mJ/cm2).
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Project description:Gene expression in wild-type and p38a-knockout dendritic cells (DCs) were compared. Lymph node dendritic cells were isolated from mice, and left unstimulated and stimulated with Pam3CSK4, a toll-like receptor 2 agonist. C57BL/6 wild-type mice, and dendritic cell-specific p38a-knockout mice on a C57BL/6 background were used for isolation of primary DCs.
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Project description:Gene expression in the colonic mucosa of wild-type and p38a-knockout intestinal epithelial cells (IECs) were compared. C57BL/6 wild-type mice, and intestinal epithelial cell-specific p38a-knockout mice on a C57BL/6 background were used for isolation of colonic mucosa Gene expression in each genotype was analyzed in triplicate.
2014-07-01 | E-GEOD-55356 | biostudies-arrayexpress
Project description:Ultraviolet (UV) light affects endocrinological and behavioral aspects of human sexuality via an unknown mechanism. Using a unique male-female comparative approach, we discovered that the sexual behavioral and hormonal features enhanced by UVB are mediated by the skin. In mice, UV exposure increases hypothalamus-pituitary-gonadal axis hormone levels, resulting in enhanced ovary size, extended estrus days, and anti-Mullerian hormone (AMH) expression. It likewise enhances the sexual responsiveness and attractiveness of females and male-female interactions of both males and females. Conditional knockout of p53 specifically in skin keratinocytes abolished UV’s effects. In humans, UV exposure enhanced romantic passion in both genders increased testosterone levels in men. Our data, revealing that UVB triggers a skin-brain-gonadal axis through skin p53 activation, offers therapeutic opportunities for sex-steroid-related dysfunctions. We speculate that during human furless skin evolution, the skin became the front-line regulator of the response to UVB.
2022-02-17 | PXD025973 | Pride
Project description:Purpose: to characterise the steady state gene expression and transcriptomic response of resident murine epidermal immune cells (dendritic epidermal T cells, DETC; Langerhans cells, LCs) and epithelial cells (interfollicualr keratinocytes) to non-microbial stress in the form of ultraviolet B (UVB) radiation Methods: 6 C57Bl/6 mice were administered 300mJ/cm^2 UVB radiation to the dorsal side of both ears 24hr prior to tissue harvest, and another 6 administered the same dose 4 hr prior. Ears were harvested and dorsal and ventral ear sheets were separated. Samples were pooled from 2 mice to generate 3 biological replicates per timepoint. Dorsal sheets were used for UV samples, while ventral sheets from 24hr UV mice were used as unchallenged skin. Epidermis was separated and digested, and epidermal populations were FACS sorted. Libraries were prepared and sequenced on an Illumina HiSeq 2500. Conclusions: these data reveal the transcriptomic response of LC, DETC and interfollicular keratinocytes to acute epithelial stress in the form of DNA damage
2021-12-12 | GSE160477 | GEO
Project description:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages.
2010-09-05 | GSE19411 | GEO
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: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:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages. Skin epidermal cells from 2 individual C57BL/6 mice and 2 individual AhR-deficient mice (deletion of exon2, AhRtm1Bra) were grown for 6-8 weeks in selection medium to propagate melanocytes.
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