Single cell RNA-seq for brain cerebral cortex transcriptome
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PROVIDER: PRJNA810030 | ENA |
REPOSITORIES: ENA
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Project description:Single cell RNA-seq for brain cerebral cortex transcriptome
| PRJNA649578 | ENA
Project description:By analyzing brain cerebral cortex transcriptome, we provide the gene expression profile from diverse cell types from brain.
2022-12-31 | GSE197360 | GEO
Project description:By analyzing brain cerebral cortex transcriptome, we provide the gene expression profile from diverse cell types from brain.
2021-12-31 | GSE155397 | GEO
Project description:We have applied a recently developed, highly accurate and sensitive single-cell RNA-seq method (STRT/C1) to perform a molecular census of two regions of the mouse cerebral cortex: the somatosensory cortex and hippocampus CA1. We isolated cells fresh from somatosensory cortex (S1) and hippocampus CA1 area of juvenile (P22 - P32) CD1 mice, 33 males and 34 females. Cells were collected without selection, except that 116 cells were obtained by FACS from 5HT3a-BACEGFP transgenic mice. A total of 76 Fluidigm C1 runs were performed, each attempting 96 cell captures and resulting in 3005 high-quality single-cell cDNAs, containing Unique Molecular Identifiers allowing counting of individual mRNA molecules, even after PCR amplification.
2015-02-20 | E-GEOD-60361 | biostudies-arrayexpress
Project description:We have applied a recently developed, highly accurate and sensitive single-cell RNA-seq method (STRT/C1) to perform a molecular census of two regions of the mouse cerebral cortex: the somatosensory cortex and hippocampus CA1.
2015-02-20 | GSE60361 | GEO
Project description:Cajal-Retzius cells have important role in cerebral cortex development, such as secreted Reln protein, maintain normal lays of cerebral cortex. To explore novel secretory protein of Cajal-Retzius cells and to survey the roles of Cajal-Retzius cells in cerebral cortex development, we analyzed transcriptome profiles of 6753 single cells of the embryonic 18 days.
2019-11-27 | GSE123035 | GEO
Project description:We analyzed transcriptomic characteristic of motor cortex from Sprague-Dawley rats brain with cerebral ischemia and reperfusion (CIR).
2024-01-12 | GSE222704 | GEO
Project description:<p><strong>BACKGROUND:</strong> The protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. However, the molecules that contribute to these changes remain largely unknown.</p><p><strong>METHODS:</strong> We have investigated the impact of T. gondii infection on the overall metabolism of mouse cerebral cortex. Mass-spectrometry-based metabolomics and multivariate statistical analysis were employed to discover metabolomic signatures that discriminate between cerebral cortex of T. gondii-infected and uninfected control mice.</p><p><strong>RESULTS:</strong> Our results identified 73, 67 and 276 differentially abundant metabolites, which were involved in 25, 37 and 64 pathways at 7, 14 and 21 days post-infection (dpi), respectively. Metabolites in the unsaturated fatty acid biosynthesis pathway were upregulated as the infection progressed, indicating that T. gondii induces the biosynthesis of unsaturated fatty acids to promote its own growth and survival. Some of the downregulated metabolites were related to pathways, such as steroid hormone biosynthesis and arachidonic acid metabolism. Nine metabolites were identified as T. gondii responsive metabolites, namely galactosylsphingosine, arachidonic acid, LysoSM(d18:1), L-palmitoylcarnitine, calcitetrol, 27-Deoxy-5b-cyprinol, L-homophenylalanine, oleic acid and ceramide (d18:1/16:0).</p><p><strong>CONCLUSIONS:</strong> Our data provide novel insight into the dysregulation of the metabolism of the mouse cerebral cortex during T. gondii infection and have important implications for studies of T. gondii pathogenesis.</p>
2020-04-23 | MTBLS770 | MetaboLights
Project description:Background: Prenatal exposure to air pollutants is associated with increased risk for neurodevelopmental and neurodegenerative disorders. However, few studies have identified transcriptional changes related to air pollutant exposure. Methods: RNA sequencing was used to examine transcriptomic changes in blood and cerebral cortex of three male and three female mouse neonates prenatally exposed to traffic-related nano-sized particulate matter (nPM) compared to three male and three female mouse neonates prenatally exposed to control filter air. Results: We identified 19 nPM-associated differentially expressed genes (nPM-DEGs) in blood and 124 nPM-DEGs in cerebral cortex. The cerebral cortex transcriptional responses to nPM suggested neuroinflammation involvement, including CREB1, BDNF, and IFN γ genes. Both blood and brain tissues showed nPM transcriptional changes related to DNA damage, oxidative stress, and immune responses. Three blood nPM-DEGs showed a canonical correlation of 0.98 with 14 nPM-DEGS in the cerebral cortex, suggesting a convergence of gene expression changes in blood and cerebral cortex. Exploratory sex-stratified analyses suggested a higher number of nPM-DEGs in female cerebral cortex than male cerebral cortex. The sex-stratified analyses identified 2 nPM-DEGs (Rgl2 and Gm37534) shared between blood and cerebral cortex in a sex-dependent manner. Conclusions: Our findings suggest that prenatal nPM exposure induces transcriptional changes in the cerebral cortex, some of which are also observed in blood. Further research is needed to replicate nPM-induced transcriptional changes with additional biologically relevant time points for brain development.
2021-08-25 | GSE142453 | GEO
Project description:Study on selective vulnerability of certain brain regions to oxidative stress. Here we selected 4 brain regions (hippocampal CA1 and CA3, cerebral cortex, and cerebellar granular layer) to study this phenomenon. Experiment Overall Design: Neurons were collected from the 4 regions of the rat brain and subjected to Affymetrix RAE230A analysis, in order to identify genes related to the differential vulnerability of the neurons to oxidative stress.
2008-04-07 | E-GEOD-7139 | biostudies-arrayexpress