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PROVIDER: PRJNA145587 | ENA |
REPOSITORIES: ENA
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Project description:Analyzing the hippocampal gene network to determine the effects of coral calcium hydride on antioxidant ability in rat brain
| PRJNA210869 | ENA
Project description:Recent studies strongly support the hypothesis that antioxidant diet inhibits the pathological aging process as shown in senescence-accelerated mouse prone 8 (SAM/P-8). In our previous study, we reported that a diet rich in antioxidants inhibits the pathological aging process, as shown coral calcium hydride (CCH) increased the endogenous antioxidant ability and contributed to prolonging the life-span of SAM/P-8. In order to test the hypothesis that antioxidant CCH supplementation to SAM/P-8 mice would change the gene expression and understand how CCH reverses the acceleration of aging in SAM/P-8 mice, in the current study, we used a DNA array to compare the expression levels in the hippocampus of the brains from 16-week-old SAM/P-8 mice treated or not treated with CCH. The most significant up regulated changes in the gene network of SAM/P-8 mice were free radical scavenging and molecular transport, and genes associated with cell death, cancer, and cell cycle were downregulated. Our findings about changes in these mRNA might be associated with that inhibition of the acceleration of aging is observed in SAM/P-8 mice fed a CCH-diet. Eight-week-old male SAM/P-8 and SAM/R-1 mice were assigned to two groups: the CCH-fed group (fed with CCH for 8 weeks with CE-2 (rodent diet, Clea Japan, Inc., Tokyo, Japan) containing 0.1% CCH) and the control group (fed with CE-2 for 8 weeks).
2011-09-22 | E-GEOD-31606 | biostudies-arrayexpress
Project description:Recent studies strongly support the hypothesis that antioxidant diet inhibits the pathological aging process as shown in senescence-accelerated mouse prone 8 (SAM/P-8). In our previous study, we reported that a diet rich in antioxidants inhibits the pathological aging process, as shown coral calcium hydride (CCH) increased the endogenous antioxidant ability and contributed to prolonging the life-span of SAM/P-8. In order to test the hypothesis that antioxidant CCH supplementation to SAM/P-8 mice would change the gene expression and understand how CCH reverses the acceleration of aging in SAM/P-8 mice, in the current study, we used a DNA array to compare the expression levels in the hippocampus of the brains from 16-week-old SAM/P-8 mice treated or not treated with CCH. The most significant up regulated changes in the gene network of SAM/P-8 mice were free radical scavenging and molecular transport, and genes associated with cell death, cancer, and cell cycle were downregulated. Our findings about changes in these mRNA might be associated with that inhibition of the acceleration of aging is observed in SAM/P-8 mice fed a CCH-diet.
2011-09-23 | GSE31606 | GEO
Project description:In our previous study, we reported that a diet rich in antioxidants such as coral calcium hydride (CCH) increased the endogenous antioxidant ability in the hippocampus of rats. We conducted this study to test the hypothesis that diet supplementation with CCH would change the gene expression in rats and to understand how CCH enhances antioxidant ability. We used a DNA array to compare the expression levels in the hippocampus of rats fed with CCH for 2 weeks with those of rats fed a normal diet. Immune response-related genes were down-regulated, while nuclear respiratory factor 2 and aldehyde dehydrogenase 3A were up-regulated. Our findings about the changes in the mRNA levels of these genes well explain the physiological finding of enhanced antioxidant ability in rat brain. CCH was obtained from ICB, Ltd., Sendai, Japan, and coral calcium (CC) was purchased from Coralbio, Okinawa, Japan. Male Wistar rats were acquired from Kyudo, Co., Ltd. and maintained at the Experimental Animal Center of the University of Miyazaki at a controlled ambient temperature of 23 ± 1 °C and 50 ± 10% relative humidity. The Committee for Ethics on Animal Experiments, Faculty of Medicine, University of Miyazaki, Japan, reviewed and approved the experimental design. Six-week-old male Wistar rats (n = 8) were assigned to 2 groups: standard diet-fed group (CE-2, Clea Japan, Inc., Tokyo, Japan) and CCH-fed group. The CCH diet was standard CE-2 feed supplemented with 0.1% CCH powder. Inhibition of accelerated aging and an increase in the in vivo antioxidant ability was observed in SAM/P-8 mice fed a diet supplemented with 0.1% CCH. In accordance with these reports, the CCH concentration used in our study was set at 0.1%.The animals were killed by cervical dislocation at the age of 8 weeks. They were decapitated and the hippocampi were removed and rapidly frozen in liquid nitrogen. The hippocampi were then homogenized with a conventional rotor-stator homogenizer. Total RNA was then extracted from the tissues by using the RNeasy Lipid Tissue Mini Kit (Qiagen, Valencia, CA).
2013-12-31 | E-GEOD-48623 | biostudies-arrayexpress
Project description:Coral skeletons are materials composed of inorganic aragonitic fibers, proteins, sugars and lipids that are highly organized to form a solid body upon which the animals live. The skeleton contains more than 30 proteins, all of which are encoded in the animal genome and secreted during the biomineralization process. How these proteins are spatially related is unknown. Using a combination of chemical crosslinking and high-resolution tandem mass spectrometry, we identify, for the first time. the spatial interactions of the skeletal proteins within a stony coral. Our subsequent network analysis revealed several coral acid-rich proteins (CARPs) are invariably associated with carbonic anhydrase(s), alpha-collagen, cadherins and other calcium binding proteins. These interactions clearly show that protein-protein interactions in coral skeletons are highly coordinated and are key to understanding the formation and persistence of coral skeletons through time
2021-01-25 | PXD020076 | Pride
Project description:Increasing seawater’s calcium concentration has shown to increase reef building (scleractinian) coral’s calcification rates. In this way the expression of the genes that are associated with the calcification process also altered and, thus can be identified. Needless to say that the overall gene repertoire that participate in the coral calcification process and its molecular mechanisms have not yet been revealed, although sporadic genes that are related to the process have been discovered and investigated. In this study, nubbins of the Red Sea scleractinian coral, Stylophora pistillata were treated with increased calcium concentrations seawater (addition of 100 gm/L) and the genes that have been up-regulated were compared to the genes expression profile of corals with natural seawater calcium concentration. Measurements of AT were taken at mid-day (11:00) and in nighttime (23:00), to record the calcification rates of coral individuals under normal and increased calcium seawater concentrations. In order to reveal the gene involved in the calcification process, S. pistillata fragments of normal and of increased calcium concentrations were sampled for microarray RNA transcriptional profiling at two time-points (mid-day and nighttime).Results of this study have revealed that Smad genes may play a role in the coral skeletal growth apparatus. This study show that the calcification molecular mechanism is conserved Among identified genes are large group of genes that are characterized in the TGF-b/BMP signal transduction pathways which have been revealed in other organisms to participate in bone and cartilage tissue development molecular processes.
2017-06-29 | GSE87159 | GEO
Project description:Background Coral reefs are expected to be severely impacted by rising seawater temperatures associated with climate change. This study used cDNA microarrays to investigate transcriptional effects of thermal stress in embryos of the coral Montastraea faveolata. Embryos were exposed to 27.5C, 29.0C, and 31.5C directly after fertilization. Differences in gene expression were measured after 12 and 48 hours. Results Analysis of differentially expressed genes indicated that increased temperatures may lead to oxidative stress, apoptosis, and a structural reconfiguration of the cytoskeletal network. Metabolic processes were downregulated, and the action of histones and zinc finger-containing proteins may have played a role in the long-term regulation upon heat stress. Conclusions Embryos responded differently depending on exposure time and temperature level. Embryos showed expression of stress-related genes already at a temperature of 29.0C, but seemed to be able to counteract the initial response over time. By contrast, embryos at 31.5C displayed continuous expression of stress genes. The genes that played a role in the response to elevated temperatures consisted of both highly conserved and coral-specific genes. These genes might serve as a basis for research into coral-specific adaptations to stress responses and global climate change. The experimental setup followed a reference design, i.e. all samples were hybridized against the same pool made up of equal amounts of RNA from all samples. We used three technical replicates for each temperature. Common reference samples were labeled with Cy3, temperature samples with Cy5. Microarrays for M. faveolata contained 1,314 coding sequences, of which 43% had functional annotations as determined by homology to known genes.
2010-05-06 | E-GEOD-15088 | biostudies-arrayexpress
Project description:Exome sequencing of senescence-accelerated mice
| PRJDB37 | ENA
Project description:Transgenic mouse models have been widely used to investigate the pathology of Alzheimer’s disease (AD). To elucidate underlying mechanisms of AD pathogenesis by amyloid beta (Aβ) and tau, we have generated a novel animal model of AD; ADLP - APT mice (Alzheimer’s Disease-Like Pathology) – carrying mutations of human amyloid precursor protein (APP), human presenilin-1 (PS1) and human tau. We profiled 9,824 proteins in the hippocampus of ADLP model mice using quantitative proteomics. To identify functional signatures in pathology of ADLP - APT mice, in-depth bioinformatics analysis was performed. For a longitudinal change of differentially expressed proteins (DEPs), we identified ADLP - APT mice hippocampal proteome in an age-dependent manner. Network maps of interactome between Aβ and tau in newly generated ADLP - APT mice reveal relationship between accelerated NFT pathology of AD and proteomic changes.
2018-01-25 | PXD006214 | Pride
Project description:The present study examines the effects of whale meat extract (WME) supplementation on the senescence-accelerated mouse prone 8 (SAMP8) model at the level of learning memory formation and gene expression profiles genome-wide. Our present study builds up on these previous studies by focusing on two sets of experiments examining WME-supplemented diet, on SAMP8 and SAMR1 (senescence-accelerated mouse resistant 1) learning and memory deficits (experiment 1) and whole-genome DNA microarray-based transcriptomics profiling in conjunction with Ingenuity Pathway Analysis (IPA) (experiment 2). We also examined the SAMP8 and SAMR1 mice fed with the regular (control; low-safflower oil, LSO) diets specifically to know the gene profiles in the brain of the SAMP8 mouse. Results revealed that WME supplementation on SAMP8 mouse resulted in an increase in the level of learning memory formation and positive changes in the transcriptome of the brain, suggested through the observation of recovery of gene expressions in the SAMP8 model over the not-supplemented mouse.
2016-01-01 | GSE76459 | GEO