The effect of corticosterone treatment on the proteome of mouse brain endothelial bEnd.3 cells
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive HF
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Cell Culture, Endothelial Cell
SUBMITTER: 
Alexei Leliavski
LAB HEAD: Gurumoorthy Krishnamoorthy
PROVIDER: PXD022166 | Pride | 2021-03-01
REPOSITORIES: Pride
Similar Datasets
Project description:Glucocorticoids are potent anti-inflammatory drugs prescribed in various diseases such as asthma, rheumatoid arthritis and multiple sclerosis. The effects of glucocorticoids have extensively been studied in immune cells. However, the regulation of inflammation by glucocorticoids in endothelial cells remains poorly understood. In this study, we stimulated murine lung endothelial cell line with dexamethasone (100 nM) and IFN-gamma (20 ng/mL) for 24 hours and extracted RNA for RNA-seq.
2017-09-11 | E-MTAB-5921 | biostudies-arrayexpress
Project description:Effect of expression of dipeptidyl peptidase-IV (DPP-IV) in U373 cell line on uncontrolled cell proliferation and aberrant interactions with the brain extracellular matrix.
2011-12-31 | E-MTAB-583 | biostudies-arrayexpress
Project description:Exposure to excessive glucocorticoids, which are major mediators of the stress reaction, is detrimental to brain development related to an increased risk of psychiatric disorders. However, the molecular mechanism underlying the effect of excessive glucocorticoids on the developing brain remains largely unclear. To clarify the mechanism, we examined the effects of glucocorticoids on cultured neuronal progenitor cells (NPCs) from cerebral cortices from rat embryo. We performed comparative analysis using gene expression profiling of corticosterone- or vehicle-treated NPCs. Results provide insight into the effects of glucocorticoids in regulating genetic programs important for controlling NPCsâ properties. Experiment Overall Design: Three couples of RNA samples from corticosterone- or vehicle-treated neuronal progenitor cells were analyzed.
2009-04-04 | E-GEOD-11478 | biostudies-arrayexpress
Project description:In all eukaryotes, histone variants are incorporated into a subset of nucleosomes to create functionally specialized regions of chromatin. One such variant, H2A.Z, replaces histone H2A and is required for viability in all metazoans tested to date. However, the function of H2A.Z in chromatin organization, transcription, and development remains controversialunclear. We mapped the genome-wide distribution of the C. elegans H2A.Z ortholog HTZ-1 during embryogenesis by Chromatin ImmunoPrecipitation on DNA microarrays (ChIP-chip). We find that H2A.Z is incorporated upstream of approximatelybout 25% of C. elegans genes, preferentially upstream of genes required for development and occupied by RNA polymerase II. Fewer sites of HTZ-1 localization occur on the X chromosome relative to autosomes, consistent with the lack of essential genes on X. The data provide evidence for unexpectedly widespread independent regulation of genes within operons. In 37% of operons, HTZ-1 is incorporated upstream of internally encoded genes. In conjunction with ChIP-chip, we used genetic mutation, RNAi, and microscopy to establish that HTZ-1 is present in every cell, and that maternally supplied HTZ-1 is essential for normal development. We interpret these results to indicate that C. elegans HTZ-1 functions in establishing or maintaining an essential chromatin state at promoters regulated dynamically during development. Keywords: chip-chip 4 independent HTZ-1 ChIP biological replicates were performed with 1 dye-swap replicate (ChIP 4). RNA Polymerase II ChIPs were performed from extracts used for HTZ-1 ChIPs 1 and 2 (RNAPII ChIP2 is a dye-swap). HTZ-1, RNA Polymerase II, and no antibody raw intensities Data were normalized by median centering log ratios (IP/input). Normalized Log2 ratios from each experiment were converted to standardized z-scores, array sets were concatenated, and then the median of experiments was taken.
2010-05-25 | E-GEOD-10201 | biostudies-arrayexpress
Project description:Exposure to excessive glucocorticoids, which are major mediators of the stress reaction, is detrimental to brain development related to an increased risk of psychiatric disorders. However, the molecular mechanism underlying the effect of excessive glucocorticoids on the developing brain remains largely unclear. To clarify the mechanism, we examined the effects of glucocorticoids on cultured neuronal progenitor cells (NPCs) from cerebral cortices from rat embryo. We performed comparative analysis using gene expression profiling of corticosterone- or vehicle-treated NPCs. Results provide insight into the effects of glucocorticoids in regulating genetic programs important for controlling NPCs’ properties. Keywords: expression analysis, corticosterone, neuronal progenitor, cortex
2009-03-31 | GSE11478 | GEO
Project description:Whole genome sequencing data of brain AVM endothelial and non-endothelial cell fractions, as well as paired blood samples
| EGAD00001009696 | EGA
Project description:An essential first step in the posttranslational modification of proteins with UFM1, UFMylation, is the proteolytic cleavage of pro-UFM1 to expose a C-terminal glycine. Of the two UFM1-specific proteases (UFSPs) identified in humans, only UFSP2 is reported to be active since the annotated sequence of UFSP1 lacks critical catalytic residues. Nonetheless, efficient UFM1 maturation occurs in cells lacking UFSP2 suggesting the presence of another active protease. We hereby identify UFSP1 translated from a non-canonical start site to be this protease. Cells lacking both UFSPs show complete loss of UFMylation resulting from an absence of mature UFM1. While UFSP2, but not UFSP1, removes UFM1 from the ribosomal subunit RPL26, UFSP1 acts earlier in the pathway to mature UFM1 and cleave a potential auto-inhibitory modification on UFC1, thereby controlling activation of UFMylation. In summary, our studies reveal distinctions in substrate specificity and localization-dependent functions for the two proteases in regulating UFMylation. The present dataset includes Data Independent Acquisition (DIA) quantitative proteomics analysis of knockout cell lines reported in our study. Our analysis of the processed data is presented in Figure-6.
2022-08-22 | PXD035142 | Pride
Project description:MicroRNAs are important negative regulators of protein coding gene expression, and have been studied intensively over the last few years. To this purpose, different measurement platforms to determine their RNA abundance levels in biological samples have been developed. In this study, we have systematically compared 12 commercially available microRNA expression platforms by measuring an identical set of 20 standardized positive and negative control samples, including human universal reference RNA, human brain RNA and titrations thereof, human serum samples, and synthetic spikes from homologous microRNA family members. We developed novel quality metrics in order to objectively assess platform performance of very different technologies such as small RNA sequencing, RT-qPCR and (microarray) hybridization. We assessed reproducibility, sensitivity, quantitative performance, and specificity. The results indicate that each method has its strengths and weaknesses, which helps guiding informed selection of a quantitative microRNA gene expression platform in function of particular study goals.
2013-09-01 | E-MTAB-1815 | biostudies-arrayexpress
Project description:Vascular inflammation is present in many cardiovascular diseases and exogenous glucocorticoids have traditionally been used as a therapy to suppress inflammation. However, recent data has shown that endogenous glucocorticoids, acting through the endothelial glucocorticoid receptor, act as negative regulators of inflammation. Here we performed chromatin immunoprecipitation for the glucocorticoid receptor followed by next-gen sequencing in mouse endothelial cells to investigate how the endothelial glucocorticoid receptor regulates vascular inflammation. We identified a novel role of the Wnt signaling pathway in this setting and show that loss of the endothelial glucocorticoid receptor results in up regulation of Wnt signaling both in vitro and in vivo using our validated mouse model. Further we demonstrate glucocorticoid receptor regulation of a key gene in the Wnt pathway via a novel glucocorticoid response element gleaned from our genomic data. These results suggest a novel role for endothelial Wnt signaling modulation in states of vascular inflammation.
2020-04-07 | GSE119092 | GEO
Project description:Vascular inflammation is present in many cardiovascular diseases and exogenous glucocorticoids have traditionally been used as a therapy to suppress inflammation. However, recent data has shown that endogenous glucocorticoids, acting through the endothelial glucocorticoid receptor, act as negative regulators of inflammation. Here we performed chromatin immunoprecipitation for the glucocorticoid receptor followed by next-gen sequencing in mouse endothelial cells to investigate how the endothelial glucocorticoid receptor regulates vascular inflammation. We identified a novel role of the Wnt signaling pathway in this setting and show that loss of the endothelial glucocorticoid receptor results in up regulation of Wnt signaling both in vitro and in vivo using our validated mouse model. Further we demonstrate glucocorticoid receptor regulation of a key gene in the Wnt pathway via a novel glucocorticoid response element gleaned from our genomic data. These results suggest a novel role for endothelial Wnt signaling modulation in states of vascular inflammation.
2020-04-07 | GSE119091 | GEO