Transcript Profiling of Different CNS Regions in Response to Experimental Restraint Stress on Rats
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE17430 | GEO | 2009/08/01
SECONDARY ACCESSION(S): PRJNA118893
REPOSITORIES: GEO
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Project description:It generally believes that moderate stress could have protective and adaptive effects, but less is known about the moderate or experimental stress on CNS in stimulated animals. This study aims to investigate the potential gene expression in nociception-related central regions induced by moderate experimental stress in rats. Rats were given moderate restrain for 50 min and using cDNA microarrays to compare different gene expression in central regions. Transcriptome profiling analysis showed that stress-related genes at acute stage were up-regulated in Arc; rhythmic process-related genes were up-regulated in PAG, while glutamine metabolism-, arginine metabolis-related genes were up-regulated in DH. At late stage, immune related genes were broadly up-regulated in the CNS regions. These results suggest that specific GO categories? genes could be regulated in the specific CNS regions correlated with relative function in response to external stimuli at the beginning period. It also suggest that moderate stress could enhance neuroendocrine and immune function in broad CNS regions at late stage, and experimental stress should be careful considered, especially in neuroendocrine and immune studies. Furthermore, Sgk1 was verified by qRT-PCR and western blot. The significant up regulation implied Sgk1 in the CNS may play an important role in the response to stress. Keywords: Transcriptome analysis Rats were exposed to moderate restrain for 50 min and nociceptive testing and returned to home cages for 1 hours or 24 hours before sacrificed, termed as restrain_nociceptive_test_group 1 (RT1) and restrain_nociceptive_test_group 24 (RT24) respectively. Subsequently analyzed their nociception-related central regions transcript profile using cDNA microarrays, the rats were without receiving restraint stress and nociceptive testing as control. The tissue of arcuate nucleus (Arc), periaqueductal gray (PAG) and dorsal horn (DH) of the fifth and sixth lumbar (L5 and L6) of five rats were selected for transcript analysis in each group. The five control rats were mixed and labeled with cy5 according to different CNS regions, each RT1 or RT24 rats were labeled with cy3.
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Project description:To address the differential response of the CNS, proteomics was applied in experimental autoimmune encephalomyelitis (EAE) mice and cuprizone (CPZ) mice in two different CNS regions
2023-09-27 | PXD037019 | JPOST Repository
Project description:Transcript Profiling of Different CNS Regions in Response to Experimental Restraint Stress on Rats
| PRJNA118893 | ENA
Project description:Genome-wide transcription profiles analysis of the heat-shocked wild-type strain under moderate (40¡C) and severe heat stress (50¡C) revealed that a large number of genes are differentially expressed after heat shock. 358 genes were up-regulated and 420 were down-regulated in response to moderate heat shock 35 (40¡C) in C. glutamicum. Our results confirmed the HrcA/CIRCE-dependent and HspR/HAIR-dependent up-regulation of chaperones following heat shock. Other genes including COG groups related to macromolecule biosynthesis and several transcriptional regulators (COG class K) were up-regulated, explaining the large number of genes affected by heat shock. Mutants having deletions in the hrcA or hspR regulators were constructed, which allowed the complete identification of the genes controlled by those systems. The up- or down-regulation of several genes observed in the microarray experiments was validated by Northern analyses and quantitative (real-time) PCR. These analyses showed the heat shock intensity-dependent response (differential response) presented by the HspR/HAIR system, in contrast with the non-differential response shown by the HrcA/CIRCE-regulated genes.
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2018-10-19 | E-MTAB-6742 | biostudies-arrayexpress
Project description:This model is from the article:
Modelling the Role of the Hsp70/Hsp90 System in the Maintenance of Protein Homeostasis
Proctor CJ, Lorimer IAJ
PLoS ONE2011; 6(7): e22038.
doi:10.1371/journal.pone.0022038,
Abstract:
Neurodegeneration is an age-related disorder which is characterised by the accumulation of aggregated protein and neuronal cell death. There are many different neurodegenerative diseases which are classified according to the specific proteins involved and the regions of the brain which are affected. Despite individual differences, there are common mechanisms at the sub-cellular level leading to loss of protein homeostasis. The two central systems in protein homeostasis are the chaperone system, which promotes correct protein folding, and the cellular proteolytic system, which degrades misfolded or damaged proteins. Since these systems and their interactions are very complex, we use mathematical modelling to aid understanding of the processes involved. The model developed in this study focuses on the role of Hsp70 (IPR00103) and Hsp90 (IPR001404) chaperones in preventing both protein aggregation and cell death. Simulations were performed under three different conditions: no stress; transient stress due to an increase in reactive oxygen species; and high stress due to sustained increases in reactive oxygen species. The model predicts that protein homeostasis can be maintained during short periods of stress. However, under long periods of stress, the chaperone system becomes overwhelmed and the probability of cell death pathways being activated increases. Simulations were also run in which cell death mediated by the JNK (P45983) and p38 (Q16539) pathways was inhibited. The model predicts that inhibiting either or both of these pathways may delay cell death but does not stop the aggregation process and that eventually cells die due to aggregated protein inhibiting proteasomal function. This problem can be overcome if the sequestration of aggregated protein into inclusion bodies is enhanced. This model predicts responses to reactive oxygen species-mediated stress that are consistent with currently available experimental data. The model can be used to assess specific interventions to reduce cell death due to impaired protein homeostasis.
Note:
Simulations were performed under three different conditions: 1) normal condition (no stress), 2) moderate stress due to an increase in reactive oxygen species (ROS) i.e. ROS levels were increased by a factor of 4 at time=4hours for a period of 1 hour (not 2 hours as mentioned in the figure 5 legend of the reference publication. This is a typo in the paper and is clarified by the author) and 3) high stress due to sustained increase in reactive oxygen species (ROS) (here ROS increases with time).
The model that corresponds to the normal condition is submitted as a main model in the BioModels Database. The other two models, that corresponds to the moderate stress conditions and high stress conditions are available in SBML format as supporting files [go to Curation tab].
Supplementary figures S3 (normal condition), S4 (moderate stress condition) and S6 (high stress condition) are reproduced here.
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Project description:A balance between cell survival and apoptosis is essential for animal development. Although proper development involves multiple interactions between germ layers, little is known about the intercellular and intertissue signaling pathways that promote cell survival in neighboring or distant germ layers . We show that serum- and glucocorticoid-inducible kinase 1 (SGK1) promoted ectodermal cell survival during early Xenopus embryogenesis through a non-cell-autonomous mechanism. Dorsal depletion of SGK1 in Xenopus embryos resulted in shortened axes and reduced head structures with defective eyes, and ventral depletion led to defective tail morphologies. Although the gene encoding SGK1 was mainly expressed in the endoderm and dorsal mesoderm, knockdown of SGK1 caused excessive apoptosis in the ectoderm. SGK1-depleted ectodermal explants showed little or no apoptosis, suggesting non-cell-autonomous effects of SGK1 on ectodermal cells. Microarray analysis revealed that SGK1 knockdown increased the expression of genes encoding FADD and caspase-10, components of the death-inducing signaling complex (DISC). Inhibition of DISC function suppressed excessive apoptosis in SGK1-knockdown embryos. SGK1 acted through the transcription factor nuclear factor kappaB to stimulate production of bone morphogenetic protein 7 (BMP7), and overexpression of BMP7 in SGK1-knockdown embryos reduced the abundance of DISC components. We show that phosphoinositide 3-kinase (PI3K) functioned upstream of SGK1, thus revealing an endodermal and mesodermal pathway from PI3K to SGK1 to NF-kappaB that produces BMP7, which provides a survival signal to the ectoderm by decreasing DISC function. To identify genes whose expression levels are regulated by SGK1 in Xenopus development, we performed genome-wide analysis by using Affymetrix GeneChip oligonucleotide microarrays. We performed two independent experiments. For each microarray experiment, we radially injected control-morpholino or xSGK1-morpholinos into 4-cell embryos, cultured the embryos until stage 12, extracted total RNAs using Trizol (Invitrogen) and purified them on RNeasy columns (Qiagen). Synthesis of cDNA, in vitro transcription and biotin labeling of cRNA, and hybridization to the Xenopus laevis genome array (Affymetrix) were performed according to the Affymetrix protocol (Two-Cycle Target Labeling Assays). Hybridized arrays were scanned using an Affymetrix GeneChip Scanner. Scanned chip images were analyzed with GeneChip Operating Software (GCOS) v. 1.4.
2011-02-21 | E-GEOD-26381 | biostudies-arrayexpress
Project description:The bovine chromaffin cell (BCC) is a unique modelM-bM-^@M-^Ta highly homogeneous and accessible neuroendocrine cellM-bM-^@M-^Tin which to study gene regulation through first messenger-initiated signaling pathways that are specific to post-mitotic cells. BCCs were treated with tumor necrosis factor (TNF) or pituitary adenylate cyclase activating polypeptide (PACAP), two critical regulators of neural cell transcriptional programming during inflammation that act on TNFR2 and PAC1 receptors, respectively, in post-mitotic neuroendocrine cells. Transcripts which were significantly up regulated by either or both first messenger were identified from microarray analysis using two bovine oligonucleotide arrays (Affymetrix and Agilent) followed by statistical analysis with Partek Genomic suite. Microarray data were combined from the two arrays using qRT-PCR sampling validation, and the first-messenger transcriptome derived from TNF and PACAP signaling were compared. More than 90 percent of the genes up regulated either by TNF or PACAP were specific to a single first messenger. BioBase suite, DIRE and Opossum were used to identify common promoter/enhancer response elements that control the expression of TNF- or PACAP-stimulated genes. Bioinformatic analysis revealed that distinct groups of transcription factors control the expression of genes up regulated by either TNF or PACAP . Most of the genes up regulated by TNF contained response elements for members of the Rel transcription factor family, suggesting TNF-TNFR2 signaling mainly through the NF-kB signaling pathway. On the other hand, the PACAP regulated genes showed no enrichment for any single response element, containing instead response elements for combinations of transcription factors allowing activation through multiple signaling pathways, including cAMP, calcium and ERK, in neuroendocrine cells. Pharmacological strategies for mimicking neuroprotection by either PACAP or TNF in the context of CNS injury or degeneration in disease might focus on individual downstream gene activation pathways to achieve greater specificity in vivo. For our analysis we have used both Affymetrix and Agilent arrays to identify the genes that are regulated up or down by neuropeptide PACAP and TNF-alpha. On Affyemetrix platform we performed technical repeats with 3 arrays with untreated samples, 3 arrays with samples from PACAP treatment, and 3 array with samples from TNF-alpha treatment. On the Agilent platform we performed technical repeats with 3 arrays for each treatment hybridizing Cy3-labelled RNA from untreated samples and Cy5-labelled RNA from either TNF-alpha or PACAP treated samples.
2012-09-01 | E-GEOD-24070 | biostudies-arrayexpress
Project description:Stress acclimation is an effective mechanism that plants acquired for adaption to dynamic environmental conditions. After undergoing cold acclimation, plants become more tolerant to cold stress. In order to understand the mechanism of cold acclimation, we performed a systematic, comprehensive study of cold response and acclimation in Cassava (Manihot esculenta), a staple crop and major food source in the tropical regions of the world. We profiled mRNA genes and small-RNA species, using next generation sequencing, and performed an integrative analysis of the transcriptome and microRNAome of Cassava across the normal condition, a moderate cold stress at 14°C, a harsh stress at 4°C after cold acclimation at 14°C, and a cold shock from 24°C to 4°C. Two results from the analysis were striking. First, the moderate stress and cold shock, despite a difference of 10°C between the two, triggered comparable degrees of perturbation to the transcriptome; in contrary, further harsh stress after cold acclimation resulted in a much smaller degree of transcriptome variation. Second and more importantly, about two thirds of the up- or down-regulated genes after moderate stress reversed their expression to down- or up-regulation, respectively, under harsh stress after cold acclimation, resulting in a genome-wide rewiring of regulatory networks. MicroRNAs, which are key post-transcriptional gene regulators, were major players in this massive rewiring of genetic circuitry. Further, a function enrichment analysis of the perturbed genes revealed that cold acclimation helped the plant to develop immunity to further harsh stress by exclusively inducing genes with functions of nutrient reservoir; in contrast, many genes with functions of viral reproduction were induced by cold shock. Our study revealed, for the first time, the molecular basis of stress acclimation in plants, and shed lights on the role of microRNA gene regulation in cold response and acclimation in Euphorbia.
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