This SuperSeries is composed of the SubSeries listed below.
HDAC inhibitors attenuate the development of hypersensitivity in models of neuropathic pain.
Specimen part
View SamplesHistone deacetylase inhibitors (HDACIs) interfere with the epigenetic process of histone acetylation and are known to have analgesic properties in models of chronic inflammatory pain. The aim of this study was to determine whether these compounds could also affect neuropathic pain. Different class I HDACIs were delivered intrathecally into rat spinal cord in models of traumatic nerve injury and antiretroviral drug-induced peripheral neuropathy (stavudine, d4T). Mechanical and thermal hypersensitivity was attenuated by 40% to 50% as a result of HDACI treatment, but only if started before any insult. The drugs globally increased histone acetylation in the spinal cord, but appeared to have no measurable effects in relevant dorsal root ganglia in this treatment paradigm, suggesting that any potential mechanism should be sought in the central nervous system. Microarray analysis of dorsal cord RNA revealed the signature of the specific compound used (MS-275) and suggested that its main effect was mediated through HDAC1. Taken together, these data support a role for histone acetylation in the emergence of neuropathic pain.
HDAC inhibitors attenuate the development of hypersensitivity in models of neuropathic pain.
Specimen part
View SamplesHistone deacetylase inhibitors (HDACIs) interfere with the epigenetic process of histone acetylation and are known to have analgesic properties in models of chronic inflammatory pain. The aim of this study was to determine whether these compounds could also affect neuropathic pain. Different class I HDACIs were delivered intrathecally into rat spinal cord in models of traumatic nerve injury and antiretroviral drug-induced peripheral neuropathy (stavudine, d4T). Mechanical and thermal hypersensitivity was attenuated by 40% to 50% as a result of HDACI treatment, but only if started before any insult. The drugs globally increased histone acetylation in the spinal cord, but appeared to have no measurable effects in relevant dorsal root ganglia in this treatment paradigm, suggesting that any potential mechanism should be sought in the central nervous system. Microarray analysis of dorsal cord RNA revealed the signature of the specific compound used (MS-275) and suggested that its main effect was mediated through HDAC1. Taken together, these data support a role for histone acetylation in the emergence of neuropathic pain.
HDAC inhibitors attenuate the development of hypersensitivity in models of neuropathic pain.
Specimen part
View SamplesPlant compensatory responses depends on transcriptional reprogramming. We used microarray analysis to understand the differential gene expression pattern between clipped (herbivore browsed)
Overcompensation in response to herbivory in Arabidopsis thaliana: the role of glucose-6-phosphate dehydrogenase and the oxidative pentose-phosphate pathway.
Specimen part
View SamplesIn this study, using a Patient Derived Xenograft (PDX) system established by transplanting primary tumors from pre-metastatic breast cancer patients we demonstrate that development of distant organ metastases correlates with the presence of Bone Marrow Disseminated Tumor Cells (BM DTCs) in the PDX mice. Comparative gene expression analysis of bone marrow (BM) from tumor bearing PDX mice which developed metastatic disease was carried out with BM from non-tumor bearing controls.
Identifying biomarkers of breast cancer micrometastatic disease in bone marrow using a patient-derived xenograft mouse model.
Specimen part
View SamplesmRNA expression in the spinal cords of the G93A-SOD1 familial ALS transgenic mouse model was compared to that in nontransgenic (Normal mouse) and transgenic mice expressing wild-type (WT)SOD1. Gene Ontology (GO)analysis was used to characterize differences in expression between G93A-SOD1 mouse and nontransgenic mouse spinal cord. Changes in multiple GO categories were found. Many of these were associated with subsystems involving cell-cell communication and intracellular signal transduction. Expression profiles of mice expressing WT-SOD1 did not differ from nontransgenic mice. In contrast, protein profiling using proteomics technology indicated changes in mitochondrial protein expression in the G93A-SOD1 mouse spinal cord that were not found in the mRNA expression analysis.
Informatics-assisted protein profiling in a transgenic mouse model of amyotrophic lateral sclerosis.
Age
View SamplesIntroduction: Mechanisms that contribute to the pathogenesis of liver damage caused by hepatitis C virus (HCV) are not fully understood. Our previous work on liver biopsies from chronic HCV patients has shown modulation of the expression of certain cell cycle proteins indicating HCV-induced modifications of cell cycle events. We therefore hypothesize that HCV infection disrupts normal regulation of cell cycle that contributes to disease progression. Objective: To identify molecular disruptions during the course of HCV-associated disease progression, using liver biopsy specimens of chronic hepatitis C patients. Methods: Liver biopsy samples classified on histological basis as early (fibrosis stage 0-1) or advanced (fibrosis stage 3-4) disease stage were studied using oligonucleotide array ( HG U133 Plus 2.0, Affymetrix GeneChip System). For comparison, liver specimens from patients with non-viral hepatitis were also analyzed by microarray. Expression data was analyzed using Genespring (GX 7.2) and Ingenuity Pathway analysis (3.0). The differential expression of selected cell cycle genes (cyclin D2, KPNA2, HERC5 and Bcl-2) identified after microarray analysis was confirmed by quantitative real-time RT-PCR. Results: Microarray analysis revealed two-fold or greater transcriptional change in 792 genes of the total 38,500 known human genes in HCV-advance disease stage (HCV-A) as compared to HCV-early disease stage (HCV-E). Most of the genes have a defined role in immune response, extracellular matrix and cell cycle and apoptosis.
Gene profiling of early and advanced liver disease in chronic hepatitis C patients.
Specimen part, Disease, Disease stage
View SamplesWe applied previously established in silico whole-embryo body (WB)-subtraction-based approach to identify “lens-enriched” genes. These new RNA-seq datasets on embryonic stages E10.5, E12.5, E14.5 and E16.5 confirmed high expression of established cataract-linked genes and identified several new potential regulators in the lens. Finally, we present lens stage-specific UCSC Genome Brower annotation-tracks; these are publicly accessible through iSyTE (https://research.bioinformatics.udel.edu/iSyTE/) and enable a user-friendly visualization of lens gene expression/enrichment to help prioritize genes from high-throughput data from cataract cases. Overall design: RNA-sequencing datasets of microdissected embyonic eye lens samples from stages embryonic day E10.5, E12.5, E14.5 and E16.5 were generated. To estimate lens enriched genes we generated control “whole-embryo body (WB)” datasets. The lens enriched genes were used for enrichment level based clustering to identify gene clusters exhibiting distinct lens enrichment patterns across E10.5 to E16.5 developmental window. This new lens RNA-seq data and its accessibility through iSyTE 2.0 serves as a new integrative resource for prioritization of lens defects and/or cataract-linked candidate genes identified by other high-throughput analyses such as exome-seq and GWAS.
RNA sequencing-based transcriptomic profiles of embryonic lens development for cataract gene discovery.
Cell line, Subject
View SamplesGene expression profile studies have identified an interferon signature in whole blood or mononuclear cell samples from patients with systemic lupus erythematosus. This study was designed to determine whether specific lymphocyte and myeloid subsets freshly isolated from the blood of systemic lupus erythematosus patients demonstrated unique gene expression profiles compared to subsets isolated from healthy controls.
Combined deficiency of proapoptotic regulators Bim and Fas results in the early onset of systemic autoimmunity.
No sample metadata fields
View SamplesWe report the transcriptional response of the zebrafish digestive organs to an acute high-fat feed using RNASeq analysis and highlight the changes in gene expression involved in the synthesis, storage, and dispersal of lipids. These key physiological responses to a high-fat meal all stem from the endoplasmic reticulum (ER), where lipids are formed and assigned to their fates. Overall design: A feeding time course was undertaken with 6.5-dpf larval zebrafish. Triplicate samples were independently prepared from pairwise crosses fed either high-fat or low-fat food. 5% egg yolk emulsion (high-fat) feeds and 10% egg white (low-fat) feeds were prepared. At the appropriate time points, digestive organs (intestine, liver, pancreas) were dissected from 10 anesthetized larval zebrafish. Unfed controls were used to determine a transcriptional baseline.
Endoplasmic Reticulum Lipid Flux Influences Enterocyte Nuclear Morphology and Lipid-dependent Transcriptional Responses.
No sample metadata fields
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