Human skin metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA553979 | ENA |
REPOSITORIES: ENA
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Project description:Epigenetic changes represent an attractive mechanism for understanding the phenotypic changes associated with human aging. Age-related changes in DNA methylation at the genome scale have been termed epigenetic drift, but the defining features of this phenomenon remain to be established. Human epidermis represents an excellent model for understanding age-related epigenetic changes because of its substantial cell-type homogeneity and its well-known age-related phenotype. We have now generated and analyzed the currently largest set of human epidermis methylomes (N=108) using array-based profiling of 450,000 methylation marks in various age groups. Data analysis confirmed that age-related methylation differences are locally restricted and characterized by relatively small effect sizes. Nevertheless, methylation data could be used to predict the chronological age of sample donors with high accuracy. We also identified discontinuous methylation changes as a novel feature of the aging methylome. Finally, our analysis uncovers an age-related erosion of DNA methylation patterns that is characterized by a reduced dynamic range and increased heterogeneity of global methylation patterns. These changes in methylation variability were accompanied by a reduced connectivity of transcriptional networks. Our findings thus define the loss of epigenetic regulatory fidelity as a key feature of the aging epigenome. This data set contains data from transcription profiling by array of human epidermis samples. The results of methylation profiling are provided in the ArrayExpress experiment E-MTAB-4385.
2016-03-24 | E-MTAB-4382 | biostudies-arrayexpress
Project description:Epigenetic changes represent an attractive mechanism for understanding the phenotypic changes associated with human aging. Age-related changes in DNA methylation at the genome scale have been termed epigenetic drift, but the defining features of this phenomenon remain to be established. Human epidermis represents an excellent model for understanding age-related epigenetic changes because of its substantial cell-type homogeneity and its well-known age-related phenotype. We have now generated and analyzed the currently largest set of human epidermis methylomes (N=108) using array-based profiling of 450,000 methylation marks in various age groups. Data analysis confirmed that age-related methylation differences are locally restricted and characterized by relatively small effect sizes. Nevertheless, methylation data could be used to predict the chronological age of sample donors with high accuracy. We also identified discontinuous methylation changes as a novel feature of the aging methylome. Finally, our analysis uncovers an age-related erosion of DNA methylation patterns that is characterized by a reduced dynamic range and increased heterogeneity of global methylation patterns. These changes in methylation variability were accompanied by a reduced connectivity of transcriptional networks. Our findings thus define the loss of epigenetic regulatory fidelity as a key feature of the aging epigenome. This data set contains data from methylation profiling by array of human epidermis samples. The results of transcription profiling by array are provided in the ArrayExpress experiment E-MTAB-4382.
2016-03-24 | E-MTAB-4385 | biostudies-arrayexpress
Project description:Intestinal calcium absorption is the sole pathway to supply calcium to the body and duodenum is the most efficient site of calcium absorption. Endurance exercise with moderate intensity significantly increased the intestinal calcium absorption. The unloaded non-impact excercise, such as swimming may enhance calcium absorption. However, the cellular and molecular mechanisms of this change have not been investigated. Thus, a genome-wide study by using microarray should reveal changes in the expression of several transporter genes in the intestinal absorptive cells of swimming excercised rats. Keywords: Gene expression; Comparative genomic hybridization Twelve rats were randomly divided into control and swimming groups. Swimming rats were initially trained for a week until they could swim non stop 1 hour/day. Swimming frequency was 5 days/week for 2 weeks. The age-matched control remained sedentary for 2 weeks in a swimming pool. At the end of the swimming protocol, the intestinal segments of rats were removed for total RNA extraction and microarray study.
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Project description:A healthy existence relationship between mussels and environment relies on suitable PH, adequate oxygen and suitable temperature. Besides ocean acidification, ocean warming has been shown to cause mussel dead, a phenomenon responsible for extensive mussel dead around the word. How heat stress impacts mussel alive is poorly understood. We founded that. The superoxide dismutase (SOD) activity of two treatment groups were significantly higher than that of control group, and the activity of acid phosphatase (ACP) was significantly higher in two treatment groups than control group. The lactate dehydrogenase (LDH) activity of 26 ℃ treatment group was significantly higher than that of control group, and the LDH activity of 33 ℃ treatment group was significantly lower than that of control group. Cellular content of lysozyme (LZM) was significantly higher in two treatment groups than control group. In this study, we applied TMT quantification to investigate how Mytilus coruscus responds to heat stress (26 ℃, 33 ℃). We identified 1652 to 1878 differentially expressed proteins (DEPs) from these heat conditions, among which 897 were commonly regulated by all the two temperature and were significantly enriched in nutrients digestion and absorption (e. g. fat digestion and absorption). Furthermore, proteins associated with nutrients metabolism, signaling pathways (p53 signaling pathway and MAPK signaling pathway)and energy metabolism (e. g. TCA cycle) were impacted, suggesting that the ability of basic metabolism of Mytilus coruscus may be altered by heat stress.
2023-05-30 | PXD035618 | Pride
Project description:The goal of this study is to check if elevated level of IL-23 and/or its downstream cytokines affect the gene expression in the jejunum of newborn mice. We engineered a mice strain in which the expression of IL-23 was directed to the keratinocytes (KSR23). The KSR23 mice had normal body weight at birth and much smaller than their control littermates at day 5. KSR23 mice died prematurely (before 15 days of age), but displayed no signs of disease in the skin, intestine, or in other organs examined. To investigate if elevated level of IL-23 and/or its downstreamcytokines could affect body growth, we examined the transcriptome of the the intestine, which are critical for the processing and absorption of nutrients. Jejunum mRNA profiles of 5-day-old WT and KSR23 were generated by deep sequencing. The transcriptome of the Jejunum of KSR23 mice at P5 differed significantly from that of their control littermates (WT). Several genes were differentially expressed, including IL-22, and genes that are downstream of it such as Reg3 genes and digestive enzymes also produced by the jejunum. Kegg pathway analysis of WT and KSR23 jejunum indicated that genes involved in protein digestion and absorption such as chymotrypsinogen B1 (Ctrb1), trypsinogen (Prss1), trypsin (Tyr5 and Tyr4), caboxypeptidase a1 (Cpa1) and chymotrypsin-like elastase family member 3b (Cela3b), were downregulated in the intestine of KSR23 mice. Transcriptome analysis also showed decreased expression of several genes involved in the regulation of the very low-density lipoprotein particle pathway (VLDL). These particles regulate fat and cholesterol release into the bloodstream. Together, these results indicate that systemic expression of IL-23, and other cytokines, correlated with significant transcriptional changes in genes that regulate food processing in the intestine.
2019-09-14 | GSE137413 | GEO
Project description:Breast cancer arising in young women has a poorer prognosis, is less likely to be hormone sensitive, and represents a particularly challenging clinical entity. The biology driving the aggressive nature of breast cancer arising in young women has yet to be defined. Among 784 patients with early stage breast cancer, using prospectively-defined, age-specific cohorts (young <= 45 years; older >= 65 years), 411 eligible patients (n = 200 < 45 years; n = 211 >= 65 years) with clinically-annotated Affymetrix microarray data were identified. Gene set enrichment analyses, signatures of oncogenic pathway deregulation and predictors of chemotherapy sensitivity were evaluated within the two age-defined cohorts. In comparing deregulation of oncogenic pathways between age groups, a statistically higher probability of PI3K (p = 0.006) and Myc (p = 0.03) pathway deregulation was observed in the tumors of younger women. When evaluating unique patterns of pathway deregulation, a low probability of Src and E2F deregulation in tumors of younger women, concurrent with activation of PI3K, Myc, and beta-catenin, conferred a worse prognosis (HR = 4.15; p = 0.008). In contrast, a higher probability of Src and E2F pathway activation in tumors of older women, concurrent low probability of PI3K, Myc and beta-catenin deregulation, was associated with a poorer outcome (HR = 2.7; p = 0.006). Similar pathway differences were identified using gene set enrichment analysis. Importantly, in multivariate analyses including clinico-pathologic variables, genomic clusters of pathway deregulation were identified to be independent predictors of disease-free survival. Finally, a significant relationship (p = 0.02) between anthracycline sensitivity and genomic clusters was observed among women aged >= 65 years. Submitters do not have approval to publish the .CEL files Experiment Overall Design: n=78
2008-06-15 | E-GEOD-7849 | biostudies-arrayexpress
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| PRJNA486190 | ENA