The hippocampus is part of a brain network essential for memory function. Paradoxically, the hippocampus is also the brain structure that is most sensitive to hypoxic-ischemic episodes. Here we show that the expression of genes associated with glycolysis and glutamate metabolism in astrocytes and the coverage of excitatory synapses by astrocytic processes undergo significant decreases in the CA1 field of the monkey hippocampus during postnatal development. Given the established role of astrocytes in the regulation of glutamate concentration in the synaptic cleft, our findings indicate that a developmental decrease in astrocytic processes underlies the selective vulnerability of CA1 during hypoxic-ischemic episodes in adulthood, its decreased susceptibility to febrile seizures with age, as well as contribute to the emergence of selective, adult-like memory function.
Developmental regulation of gene expression and astrocytic processes may explain selective hippocampal vulnerability.
Specimen part
View SamplesWe report the single-cell RNA sequencing data obtained from MDA-MB-231 breast cancer cells cultured in standard DMEM with 25 mM glucose, or adapted to culture in DMEM with 10 mM fructose to reduce glycolysis, and then cultured as mammospheres Overall design: Examination of transcriptomic changes in MDA-MB-231 breast cancer cells mammospheres in response to restriction of glycolysis
The effects of restricted glycolysis on stem-cell like characteristics of breast cancer cells.
Cell line, Subject
View SamplesWe performed micrarrays to investigate neuronal gene expression changes during acute inflammatory CNS axon injury using the murine myelin oligodendrocyte glycoprotein 35-55 (MOG35-55)-induced experimental autoimmune encephalomyelitis (EAE) model. The present study was assigned to assess the direct and indirect endogenous neuronal response to spinal axonal injury in the motor and sensory cortex.
Axonally derived matrilin-2 induces proinflammatory responses that exacerbate autoimmune neuroinflammation.
Sex, Specimen part, Treatment
View SamplesNeuroinflammatory and neuroimmune mechanisms, as exemplified by infiltrating immune cells and activation of resident endothelial/glial cells, respectively, are known to be involved in the establishment and maintenance of chronic pain. An immune system pathway that may be involved in the activation of both immune and glial cells is complement. The complement pathway is made up of a large number of distinct plasma proteins which react with one another to opsonize pathogens and induce a series of inflammatory responses to help fight infection. Cleaved products and complexes produced by complement activation are responsible for a range of effects including mediation of immune infiltration, activation of phagocytes, opsonization/lysis of pathogens and injured cells, and production of vasoactive amines such as histamine and serotonin.
Complement activation in the peripheral nervous system following the spinal nerve ligation model of neuropathic pain.
No sample metadata fields
View SamplesFN044, FN211, FN242 and FN303 are the fast neutron generated mutants in cv. Steptoe background. These 4 mutants have lesion mimic phenotype and increase disease resistance to stem rust. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, ling zhang. The equivalent experiment is BB54 at PLEXdb.]
A cation/proton-exchanging protein is a candidate for the barley NecS1 gene controlling necrosis and enhanced defense response to stem rust.
Specimen part
View SamplesThis study aims at isolate a subpopulation of thymic epithelial cells (TECs) enrich in thymic epithelial progenitors. While recent studies have shown that bipotent TEC progenitors exist in adults, the identity of thymic epithelial progenitors (TEPCs) is still debated. Using an exclusively in vivo approach, we show that quiescent UEA1– TECs actively proliferate during thymic regeneration in 6-month-old mice and possessed a MHCIIlo Sca1hi CD49fhi CD24lo Plet1– phenotype. We then performed RNA sequencing of UEA1- quiescent (label-retaining cells, called LRCs) cells and compared them to UEA1- GFP- (nonquiescent, NonLRCs) TECs. Overall design: We analyzed 2 samples with one replicate each. Each sample contains pooled cells isolated from 11 mice to reach a minimum of 10000 cells/replicate.
Detection of Quiescent Radioresistant Epithelial Progenitors in the Adult Thymus.
Specimen part, Subject
View SamplesWe have develop a proteogenomics-based approach for identification of human MHC class I-associated peptides, including those deriving from polymorphisms, mutations and non-canonical reading frames Overall design: RNA-seq of human EBV-infected B lymphoblasts derived from peripheral blood mononuclear cells from volunteers Please note that GSM1641204 and GSM1641205 are reanalyzed and duplicated sample records of GSM1186811 and GSM1186812, respectively, for the convenient retrieval of the complete raw data from SRA
Global proteogenomic analysis of human MHC class I-associated peptides derived from non-canonical reading frames.
No sample metadata fields
View SamplesAs duodenum is an important Vitamin D target organ, transcriptomic analyses were performed in this tissue.
A vitamin D receptor selectively activated by gemini analogs reveals ligand dependent and independent effects.
Age, Specimen part
View SamplesWe have generated RNA-seq of ILC2 progenitors form WT bone marrow mice. Overall design: Sorted ILC2p from 8 week-old mice were analysed in RNA-seq. Each replicate is a pool of 8 mice.
Androgen signaling negatively controls group 2 innate lymphoid cells.
Specimen part, Cell line, Subject
View SamplesTranscriptional microarray analysis was conducted on gastrocnemius muscle of control and PGC-1(i)skm-/- mice one week after the last tamoxifen administration using the Affymetrix Mouse Gene 1.0 ST.
The transcriptional coregulator PGC-1β controls mitochondrial function and anti-oxidant defence in skeletal muscles.
Specimen part
View Samples