Excessive inflammation within the central nervous system is injurious, but an immune response is also required for its repair. Macrophages are versatile cells that adopt different properties depending upon their microenvironment. Exposing macrophages to interleukin-4 and -13 (IL4/IL13) has incurred interest for their reparative properties. Unexpectedly, while macrophages exposed to the classic pro-inflammatory signals (interferon-γ/lipopolysaccharide, IFN/LPS) killed neurons and oligodendrocytes in culture, the addition of LPS to IL4/IL13-treated macrophages profoundly elevated IL10, repair metabolites (lactate, ornithine), glucose metabolism and the oligodendrocyte-trophic heparin-binding epidermal growth factor (HBEGF); cells did not display pro-inflammatory or neurotoxic features.
No associated publication
Specimen part, Treatment
View SamplesAnalyses of six Ts1Cje (Down syndrome) and six normal littermate (2N) mouse brains at postnatal day 0.
Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.
No sample metadata fields
View SamplesAnalyses of six Ts1Cje (Down syndrome) and six normal littermate (2N) mouse brains at postnatal day 0.
Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.
No sample metadata fields
View SamplesAnalyses of six Ts1Cje (Down syndrome) and six normal littermate (2N) mouse brains at postnatal day 0.
Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.
No sample metadata fields
View SamplesActivation of A Disintegrin and A Metalloprotease Domain17 (ADAM17) is involved in nephropathy, but the role of this metalloprotease and its inhibitor TIMP3 in diabetic kidney disease is unclear. We used microarray profiling to find genes differentially expressed in the 2 genotypes which could explain the more severe diabetic kidney disease features observed in T3-/- mice compared to the WT littermates.
No associated publication
Sex, Specimen part
View SamplesTranscriptome analysis of post-mortem brain tissue specimens from three brain regions (BRs), entorinal, temporal and frontal cortices, of 71 Japanese brain-donor subjects to identify genes relevant to the expansion of neurofibrillary tangles. In total, 213 brain tissue specimens (= 71 subjects 3 BRs) were involved in this study. The spreading of neurofibrillary tangles (NFTs), intraneuronal aggregates of highly phosphorylated microtubule-associated protein tau, across the human brain is correlated with the cognitive severity of Alzheimers disease (AD). To identify genes relevant to NFT expansion defined by the Braak stage, we conducted exon array analysis with an exploratory sample set consisting of 213 human post-mortem brain tissue specimens from the entorinal, temporal and frontal cortices of 71 brain-donor subjects: Braak NFT stages 0 (N = 13), III (N = 20), IIIIV (N = 19) and VVI (N = 19). We identified eight genes, RELN, PTGS2, MYO5C, TRIL, DCHS2, GRB14, NPAS4 and PHYHD1, associated with the Braak stage. The expression levels of three genes, PHYHD1, MYO5C and GRB14, exhibited reproducible association on real-time quantitative PCR analysis. In another sample set, including control subjects (N = 30) and patients with late-onset AD (N = 37), dementia with Lewy bodies (N = 17) and Parkinson disease (N = 36), the expression levels of two genes, PHYHD1 and MYO5C, were obviously associated with late-onset AD. Proteinprotein interaction network analysis with a public database revealed that PHYHD1 interacts with MYO5C via POT1, and PHYHD1 directly interacts with amyloid beta-peptide 42. It is thus likely that functional failure of PHYHD1 and MYO5C could lead to AD development.
Genes associated with the progression of neurofibrillary tangles in Alzheimer's disease.
Sex, Specimen part, Subject
View SamplesGenome-wide transcriptional profiling allows characterization of the molecular underpinnings of neocortical organization, including cortical areal specialization, laminar cell type diversity and functional anatomy. Microarray analysis of individual cortical layers across sensorimotor and association cortices in rhesus macaque demonstrated robust and specific laminar and areal molecular signatures driven by differential expression of genes associated with specialized neuronal function. Gene expression corresponding with laminar architecture was generally similar across cortical areas, although genes with robust areal patterning were often highly laminar as well, and these patterns were more highly conserved between macaque and human as compared to mouse. Layer 4 of primate primary visual cortex displayed a distinct molecular signature compared to other cortical regions, a specialization not observed in mouse. Overall, transcriptome-based relationships were strongest between proximal layers in a cortical area, and between neighboring areas along the rostrocaudal axis, reflecting in vivo cortical spatial topography and therefore a developmental imprint.
Transcriptional architecture of the primate neocortex.
Sex, Specimen part, Disease
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Mesenchymal differentiation mediated by NF-κB promotes radiation resistance in glioblastoma.
Specimen part, Treatment
View SamplesWe sought to find molecular signatures of the SGZ cell types, and to characterize the molecular pathways and transcription factor cascades that define the neurogenic niche. We used laser capture microdissection and DNA microarrays to profile gene expression in the inner (SGZ) and outer portions of the dentate gyrus (DG). Since the vast majority of the cells in the DG are mature granule cells, we compared the expression of the inner and outer portions to reveal molecular markers for the less numerous populations of the SGZ.
Conserved molecular signatures of neurogenesis in the hippocampal subgranular zone of rodents and primates.
Sex, Specimen part
View Samples