This SuperSeries is composed of the SubSeries listed below.
Interacting chemokine signals regulate dendritic cells in acute brain injury.
Sex, Specimen part
View SamplesWe inflicted TBI to wildetype (wt) mice in order to establish whether the anti-inflammatory agent cyclophosphamide can be used therapeutically.
Interacting chemokine signals regulate dendritic cells in acute brain injury.
Sex, Specimen part
View SamplesWe inflicted TBI to chemokine-deficient mouse lines in order to establish involvement of various signalling pathways that may be addressed therapeutically.
Interacting chemokine signals regulate dendritic cells in acute brain injury.
Sex, Specimen part
View SamplesISCOM vaccines induce a balanced Th1/Th2 response and cytotoxic T lymphocytes. The adjuvant component, ISCOM-Matrix, consists of purified saponin fractions, cholesterol and phospholipids. The mode of action for the ISCOM-Matrix is known to some extent but still we lack knowledge of important segments in initiation of the immune response. The study was performed to analyze the early transcriptional responses to the ISCOM-Matrix alone, without the use of co-administered antigen. Matrix M (AbISCO 100) was given as intramuscular injection and after 24 hours the pigs was sacrificed for gene expression analysis, performed for the injection site and the draining lymph node.
Global transcriptional response to ISCOM-Matrix adjuvant at the site of administration and in the draining lymph node early after intramuscular injection in pigs.
Sex, Age, Specimen part, Treatment
View SamplesThis study takes on the problem of bridging transcriptional data to neuronal phenotype and function by using publicly available datasets characterizing distinct neuronal populations based on gene expression, electrophysiology and morphology. In addition, a non-published PatchSeq dataset of Pvalb-cre positive cells in CA1 was used, which is the dataset submitted here. Taken together, these datasets were used to identify cross-cell type correlations between these data modalities. Detected correlations were classified as “class-driven” if they could be explained by differences between excitatory and inhibitory cell classes, or “non-class driven” if they could be explained by gradient like phenotypic differences within cell classes. Some genes whose relationships to electrophysiological or morphological properties were found to to be specific to either excitatory or inhibitory cell types. The Patch Seq data specifically allowed simultaneous single-cell characterization of gene expression and electrophysiology, showing that the gene-property correlations observed across cell types were further predictive of within-cell type heterogeneity. Overall design: Patchseq data was collected from single cells of the mouse hippocampus CA1 in order to investigate correlations between gene expression patterns and electrophysiological properties of various interneuron cell classes 19 individual cells Re-analysis details included in supplementary file readme.txt.
Transcriptomic correlates of electrophysiological and morphological diversity within and across excitatory and inhibitory neuron classes.
Age, Specimen part, Subject
View SamplesPatients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in individuals with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (p<0.0001) were found to be up-regulated in platelets from SLE patients as compared to healthy volunteers. Notably, patients with a history of vascular disease had increased expression of type I IFN-regulated proteins as well as more activated platelets as compared with patients without vascular disease. We suggest that interferogenic immune complexes stimulate production of IFN which up-regulates the megakaryocytic type I IFN-regulated genes and proteins. This could affect platelet activation and contribute to development of vascular disease in SLE. In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE.
Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease.
Sex, Age, Specimen part, Disease
View SamplesIn order to investigate how electrophysiological properties vary within the Pthlh population in the dorsolateral striatum we performed PatchSeq analysis of neurons labeled in 5HT3a(EGFP) and Pvalb(cre)::RCE/tdTomato mouse lines, which included Th, Npy/Mia, Cck, and Cck/Vip expressing cells. Overall design: 98 FACS-sorted single cells isolated from the dorso-lateral striatum from either a 5ht3a-EGFP mouse line or a Lhx6-cre mouse crossed onto a R26R-tdTomato reporter mouse line
Diversity of Interneurons in the Dorsal Striatum Revealed by Single-Cell RNA Sequencing and PatchSeq.
Specimen part, Cell line, Subject
View SamplesWe studied the synaptic activity-regulated gene expression response in the human genetic background using cultured human iPSC-derived (hiPSCd) neuronal networks and networks of hiPSCd neurons mixed with mouse primary neurons. Our results confirm that genetic changes affect the synaptic activity-regulated gene program, proposing a functional mechanism how they have driven evolution of human cognitive abilities. Overall design: We compared RNA profiles of untreated hiPSCd neurons and hiPSCd neurons treated with bicuculline and 4-aminopyridine for 1 or 4 hours. Samples were collected from hiPSCd neuron-only cultures and from co-cultures of hiPSCd neurons and mouse primary hippocampal neurons.
Networks of Cultured iPSC-Derived Neurons Reveal the Human Synaptic Activity-Regulated Adaptive Gene Program.
Specimen part, Subject
View SamplesThe formation of long-term memory requires signaling from the synapse to the nucleus to mediate neuronal activity-dependent gene transcription. Synapse-to-nucleus communication is initiated by influx of calcium ions through synaptic NMDA receptors and/or L-type voltage-gated calcium channels and involves the activation of transcription factors by calcium/calmodulin signaling in the nucleus. Recent studies have drawn attention to a new family of transcriptional regulators, the so-called calmodulin-binding transcription activator (CAMTA) proteins. CAMTAs are expressed at particularly high levels in the mouse and human brain, and we reasoned that, as calmodulin-binding transcription factors, CAMTAs may regulate the formation of long-term memory by coupling synaptic activity and calcium/calmodulin signaling to memory-related transcriptional responses. This hypothesis is supported by genetic studies that reported a correlation between CAMTA gene polymorphisms or mutations and cognitive capability in humans. Here, we show that acute knock-down of CAMTA1, but not CAMTA2, in the hippocampus of adult mice results in impaired performance in two memory tests, contextual fear conditioning and object-place recognition test. Short-term memory and neuronal morphology were not affected by CAMTA knock-down. Gene expression profiling in the hippocampus of control and CAMTA knock-down mice revealed a number of putative CAMTA1 target genes related to synaptic transmission and neuronal excitability. Patch clamp recordings in organotypic hippocampal slice cultures provided further evidence for CAMTA1-dependent changes in electrophysiological properties. In summary, our study provides experimental evidence that confirms previous human genetic studies and establishes CAMTA1 as a regulator of long-term memory formation. Overall design: We compared the mRNA expression profile of three groups, i.e. mice infected with a recombinant adeno-associated virus (rAAV) expressing a non-targeting control shRNA, mice infected with a rAAV expressing Camta1 targeting shRNA sequence A, and mice infected with a rAAV expressing Camta1 targeting shRNA sequence B. Three animals were used per group.
The calmodulin-binding transcription activator CAMTA1 is required for long-term memory formation in mice.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Cytomegalovirus Immediate-Early Proteins Promote Stemness Properties in Glioblastoma.
Specimen part
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