Circadian change of genes expressed in mice epidermis
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ABSTRACT:
PROVIDER: PRJNA728641 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Circadian rhythms are known to observed in all organs in mice. Skin is composed of epidermis, dermis, and subcutaneous tissue. Daily changes of epidermal genes are examined in mice. The epidermis acts as a primary barriers of the external pathogens invading into the organism. Gene expression profiles identified many bioactive substances showed daily rhythms including clock genes.
2022-05-10 | GSE174155 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE38622: Bmal1 controls circadian cell proliferation and susceptibility to UVB-induced DNA damage in the epidermis [telogen]. GSE38623: Bmal1 controls circadian cell proliferation and susceptibility to UVB-induced DNA damage in the epidermis [Anagen] GSE38624: Bmal1 controls circadian cell proliferation and susceptibility to UVB-induced DNA damage in the epidermis [Bmal1 KO] Refer to individual Series
2012-08-01 | E-GEOD-38625 | biostudies-arrayexpress
Project description:While several physiological skin parameters vary in a circadian manner, the identity of genes participating in chronobiology of skin remains unknown, leading us to define the circadian transcriptome of mouse skin at two different stages of the hair cycle, telogen and anagen. The circadian transcriptomes of telogen and anagen skin are largely distinct, with the former dominated by genes involved in cell proliferation and metabolism. The expression of many metabolic genes is antiphasic to cell cycle related genes, the former peaking during the day and the latter peaking at the night. Consistently, accumulation of reactive oxygen species, a byproduct of oxidative phosphorylation, and S-phase are antiphasic to each other in telogen skin. Furthermore, the circadian variation in S-phase is controlled by BMAL1 intrinsic to keratinocytes as keratinocyte-specific deletion of Bmal1 obliterates time of day dependent synchronicity of cell division in the epidermis leading to a constitutively elevated cell proliferation. Consistent with higher cellular susceptibility to UV-induced DNA damage during S phase, we found that mice are most sensitive to UVB-induced DNA damage in the epidermis at night. As maximum numbers of keratinocytes go through S phase in the late afternoon in the human epidermis, we speculate that in humans the circadian clock imposes regulation of epidermal cell proliferation such that skin is at a particularly vulnerable stage during times of maximum UV exposure, thus contributing to the high incidence of human skin cancers. Whole skin was collected at 4 hour intervals for 48 hours. Where ZT number indicates the number of hours elapsed from when lights are switched on. ZT0 = lights on (6am). ZT12=lights off (6pm). Total RNA was purified from the skin of each mouse and equal amount of RNA from the 3 replicates for each time point were pooled. Telogen samples were collected from skin of P46 male mice.
2012-08-01 | E-GEOD-38622 | biostudies-arrayexpress
Project description:While several physiological skin parameters vary in a circadian manner, the identity of genes participating in chronobiology of skin remains unknown, leading us to define the circadian transcriptome of mouse skin at two different stages of the hair cycle, telogen and anagen. The circadian transcriptomes of telogen and anagen skin are largely distinct, with the former dominated by genes involved in cell proliferation and metabolism. The expression of many metabolic genes is antiphasic to cell cycle related genes, the former peaking during the day and the latter peaking at the night. Consistently, accumulation of reactive oxygen species, a byproduct of oxidative phosphorylation, and S-phase are antiphasic to each other in telogen skin. Furthermore, the circadian variation in S-phase is controlled by BMAL1 intrinsic to keratinocytes as keratinocyte-specific deletion of Bmal1 obliterates time of day dependent synchronicity of cell division in the epidermis leading to a constitutively elevated cell proliferation. Consistent with higher cellular susceptibility to UV-induced DNA damage during S phase, we found that mice are most sensitive to UVB-induced DNA damage in the epidermis at night. As maximum numbers of keratinocytes go through S phase in the late afternoon in the human epidermis, we speculate that in humans the circadian clock imposes regulation of epidermal cell proliferation such that skin is at a particularly vulnerable stage during times of maximum UV exposure, thus contributing to the high incidence of human skin cancers. Whole skin was collected at 4 hour intervals for 48 hours. ZT number indicates the number of hours elapsed from when lights are switched on. ZT0 = lights on (6am). ZT12=lights off (6pm). Total RNA was purified from the skin of each mouse and equal amount of RNA from the 3 replicates for each time point were pooled. Anagen samples were collected from skin of P30 male mice.
2012-08-01 | E-GEOD-38623 | biostudies-arrayexpress
Project description:While several physiological skin parameters vary in a circadian manner, the identity of genes participating in chronobiology of skin remains unknown, leading us to define the circadian transcriptome of mouse skin at two different stages of the hair cycle, telogen and anagen. The circadian transcriptomes of telogen and anagen skin are largely distinct, with the former dominated by genes involved in cell proliferation and metabolism. The expression of many metabolic genes is antiphasic to cell cycle related genes, the former peaking during the day and the latter peaking at the night. Consistently, accumulation of reactive oxygen species, a byproduct of oxidative phosphorylation, and S-phase are antiphasic to each other in telogen skin. Furthermore, the circadian variation in S-phase is controlled by BMAL1 intrinsic to keratinocytes as keratinocyte-specific deletion of Bmal1 obliterates time of day dependent synchronicity of cell division in the epidermis leading to a constitutively elevated cell proliferation. Consistent with higher cellular susceptibility to UV-induced DNA damage during S phase, we found that mice are most sensitive to UVB-induced DNA damage in the epidermis at night. As maximum numbers of keratinocytes go through S phase in the late afternoon in the human epidermis, we speculate that in humans the circadian clock imposes regulation of epidermal cell proliferation such that skin is at a particularly vulnerable stage during times of maximum UV exposure, thus contributing to the high incidence of human skin cancers.
2012-08-02 | GSE38623 | GEO
Project description:While several physiological skin parameters vary in a circadian manner, the identity of genes participating in chronobiology of skin remains unknown, leading us to define the circadian transcriptome of mouse skin at two different stages of the hair cycle, telogen and anagen. The circadian transcriptomes of telogen and anagen skin are largely distinct, with the former dominated by genes involved in cell proliferation and metabolism. The expression of many metabolic genes is antiphasic to cell cycle related genes, the former peaking during the day and the latter peaking at the night. Consistently, accumulation of reactive oxygen species, a byproduct of oxidative phosphorylation, and S-phase are antiphasic to each other in telogen skin. Furthermore, the circadian variation in S-phase is controlled by BMAL1 intrinsic to keratinocytes as keratinocyte-specific deletion of Bmal1 obliterates time of day dependent synchronicity of cell division in the epidermis leading to a constitutively elevated cell proliferation. Consistent with higher cellular susceptibility to UV-induced DNA damage during S phase, we found that mice are most sensitive to UVB-induced DNA damage in the epidermis at night. As maximum numbers of keratinocytes go through S phase in the late afternoon in the human epidermis, we speculate that in humans the circadian clock imposes regulation of epidermal cell proliferation such that skin is at a particularly vulnerable stage during times of maximum UV exposure, thus contributing to the high incidence of human skin cancers.
2012-08-02 | GSE38622 | GEO
Project description:While several physiological skin parameters vary in a circadian manner, the identity of genes participating in chronobiology of skin remains unknown, leading us to define the circadian transcriptome of mouse skin at two different stages of the hair cycle, telogen and anagen. The circadian transcriptomes of telogen and anagen skin are largely distinct, with the former dominated by genes involved in cell proliferation and metabolism. The expression of many metabolic genes is antiphasic to cell cycle related genes, the former peaking during the day and the latter peaking at the night. Consistently, accumulation of reactive oxygen species, a byproduct of oxidative phosphorylation, and S-phase are antiphasic to each other in telogen skin. Furthermore, the circadian variation in S-phase is controlled by BMAL1 intrinsic to keratinocytes as keratinocyte-specific deletion of Bmal1 obliterates time of day dependent synchronicity of cell division in the epidermis leading to a constitutively elevated cell proliferation. Consistent with higher cellular susceptibility to UV-induced DNA damage during S phase, we found that mice are most sensitive to UVB-induced DNA damage in the epidermis at night. As maximum numbers of keratinocytes go through S phase in the late afternoon in the human epidermis, we speculate that in humans the circadian clock imposes regulation of epidermal cell proliferation such that skin is at a particularly vulnerable stage during times of maximum UV exposure, thus contributing to the high incidence of human skin cancers. Whole skin was collected at ZT22. Where ZT number indicates the number of hours elapsed from when lights are switched on. ZT0 = lights on (6am). ZT12=lights off (6pm). Het mice designate a presence of one Bmal1 mutant allele and one wt allele. KO mice designate mice germline deleted for both copies of Bmal1 allele. Total RNA was purified from the skin of each biological littermate replicate.
2012-08-01 | E-GEOD-38624 | biostudies-arrayexpress
Project description:While several physiological skin parameters vary in a circadian manner, the identity of genes participating in chronobiology of skin remains unknown, leading us to define the circadian transcriptome of mouse skin at two different stages of the hair cycle, telogen and anagen. The circadian transcriptomes of telogen and anagen skin are largely distinct, with the former dominated by genes involved in cell proliferation and metabolism. The expression of many metabolic genes is antiphasic to cell cycle related genes, the former peaking during the day and the latter peaking at the night. Consistently, accumulation of reactive oxygen species, a byproduct of oxidative phosphorylation, and S-phase are antiphasic to each other in telogen skin. Furthermore, the circadian variation in S-phase is controlled by BMAL1 intrinsic to keratinocytes as keratinocyte-specific deletion of Bmal1 obliterates time of day dependent synchronicity of cell division in the epidermis leading to a constitutively elevated cell proliferation. Consistent with higher cellular susceptibility to UV-induced DNA damage during S phase, we found that mice are most sensitive to UVB-induced DNA damage in the epidermis at night. As maximum numbers of keratinocytes go through S phase in the late afternoon in the human epidermis, we speculate that in humans the circadian clock imposes regulation of epidermal cell proliferation such that skin is at a particularly vulnerable stage during times of maximum UV exposure, thus contributing to the high incidence of human skin cancers.
2012-08-02 | GSE38624 | GEO
Project description:RNAseq analysis was performed to analyze the genes expressed in whole epidermis and upper layer epidermis (SG1 and SG2 cells) isolated from adult mouse ear.
2021-04-13 | GSE168011 | GEO
Project description:Genome-wide expression analysis of two circadian oscillatory mechanisms in the mouse liver; To identify the genes of which the circadian expression is regulated by endogenous glucocorticoids, we performed DNA microarray analysis using hepatic RNA from adrenalectomized (ADX) and sham-operated mice. Mice were housed in a 12:12 h light-dark cycle (LD12:12; lights on at zeitgeber time (ZT) 0) for at least two weeks before the day of the experiment. Liver samples were dissected, quickly frozen, and stored in liquid nitrogen. Total RNA was purified from pools of 3 animal tissues collected at each time-point using ISOGEN (Nippon Gene Co., Ltd., Japan). Hybridization to Affymetrix GeneChip (MG-U74Av2) arrays proceeded as described (Oishi K et al., J Biol Chem, 278, 41519-41527, 2003). The average difference (AD) value for each gene was provided by GeneChip software. To identify putative glucocorticoid-regulated circadian genes, we compared AD values between two time points (ZT2 and ZT14) in sham operated and in ADX mice. We applied three criteria to the selection of putative glucocorticoid-regulated circadian genes: (i) the AD value is marked as âpresentâ by the GeneChip software in at least one of two time points, (ii) the AD value exhibits a 2-fold or greater change in sham-operated mice and (iii) the fold change is below 2-fold in ADX mice. We identified 169 genes that fluctuated between day and night in the livers of sham-operated mice. Among these, 100 lost circadian rhythmicity in ADX mice. On the other hand, the circadian expression of clock or clock-related genes such as mPer2 and DBP remained almost totally intact in the liver of ADX mice. The present study showed that the circadian expression of one type of liver genes in the mouse is governed by core components of the circadian clock such as CLOCK and BMAL1, and the other depends on endogenous glucocorticoids.
2008-06-12 | E-GEOD-2162 | biostudies-arrayexpress