Arbitrary Ca2+-dependent expression data from mouse vascular endothelial cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE214156 | GEO | 2022/12/28
REPOSITORIES: GEO
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Similar Datasets
Project description:Arbitrary Ca2+-dependent expression data from mouse vascular endothelial cells
| PRJNA884267 | ENA
Project description:Altered Ca2+ handling has both immediate physiological effects and long-term genomic effects on vascular smooth muscle function. Previously we have shown that elevation of cytoplasmic Ca2+ through voltage-dependent Ca2+ channels (VDCCs) or store-operated Ca2+ channels (SOCCs) results in phosphorylation of the Ca2+/cAMP response element binding protein (CREB) in cerebral arteries. Here we demonstrate that stimulation of these different Ca2+ influx pathways results in transcriptional activation of a distinct, yet overlapping set of genes, and that the induction of selected CRE-regulated genes is prevented by the addition of corresponding Ca2+ channel blockers. Using oligonucleotide array analysis, changes in mRNA levels were quantified following membrane depolarization with K+ or depletion of intracellular Ca2+ stores with thapsigargin in human cerebral vascular smooth muscle cells. Array results for differentially regulated genes containing a CRE were confirmed by quantitative RT-PCR, and corresponding changes in protein expression were shown by Western blot analysis and immunofluorescence. Membrane depolarization induced a transient increase in c-fos mRNA and a sustained increase in early growth response-1 (Egr-1) mRNA and protein that were inhibited by application of the VDCC blocker, nimodipine, and the SOCC inhibitor, 2-aminoethoxydiphenylborate (2-APB). Thapsigargin induced a sustained increase in c-fos mRNA and MAP kinase phosphatase-1 (MKP-1) mRNA and protein, and these effects were decreased by 2-APB but not by nimodipine. Our findings thus indicate that Ca2+ entry through VDCCs and SOCCs can differentially regulate CRE-containing genes in vascular smooth muscle and imply that signals involved in growth modulation are both temporally and spatially regulated by Ca2+. Keywords: stress response
2006-03-16 | GSE2883 | GEO
Project description:Altered Ca2+ handling has both immediate physiological effects and long-term genomic effects on vascular smooth muscle function. Previously we have shown that elevation of cytoplasmic Ca2+ through voltage-dependent Ca2+ channels (VDCCs) or store-operated Ca2+ channels (SOCCs) results in phosphorylation of the Ca2+/cAMP response element binding protein (CREB) in cerebral arteries. Here we demonstrate that stimulation of these different Ca2+ influx pathways results in transcriptional activation of a distinct, yet overlapping set of genes, and that the induction of selected CRE-regulated genes is prevented by the addition of corresponding Ca2+ channel blockers. Using oligonucleotide array analysis, changes in mRNA levels were quantified following membrane depolarization with K+ or depletion of intracellular Ca2+ stores with thapsigargin in human cerebral vascular smooth muscle cells. Array results for differentially regulated genes containing a CRE were confirmed by quantitative RT-PCR, and corresponding changes in protein expression were shown by Western blot analysis and immunofluorescence. Membrane depolarization induced a transient increase in c-fos mRNA and a sustained increase in early growth response-1 (Egr-1) mRNA and protein that were inhibited by application of the VDCC blocker, nimodipine, and the SOCC inhibitor, 2-aminoethoxydiphenylborate (2-APB). Thapsigargin induced a sustained increase in c-fos mRNA and MAP kinase phosphatase-1 (MKP-1) mRNA and protein, and these effects were decreased by 2-APB but not by nimodipine. Our findings thus indicate that Ca2+ entry through VDCCs and SOCCs can differentially regulate CRE-containing genes in vascular smooth muscle and imply that signals involved in growth modulation are both temporally and spatially regulated by Ca2+. Experiment Overall Design: each of three experiments cell cultures were split three ways; one of the resulting samples was left untreated (C), another was treated with thapsigargin (TG), and the third was treated with elevated K+ (K). The resulting nine samples were used for triplicate estimates of the response of each gene to TG and K treatments. Experiment Overall Design: We tested the prospective hypothesis that genes having a CRE are differentially expressed after TG or K treatment using a permutation test: each of the 22,283 probe sets on the Affymetrix GeneChip was categorized two ways based on 1) whether or not it contains a CRE or not . Independence of CRE and threshold differential expression was rejected by Fisherâs exact test for both TG treatment ( ) and K treatment ( ). Target genes (c-fos, egr-1, and mkp-1 ) were identified based on ranking.
2009-04-29 | E-GEOD-2883 | biostudies-arrayexpress
Project description:Elevation of intracellular Ca2+ ([Ca2+]i) activates Ca2+/calmodulin-dependent kinases (CaMK) and promotes gene transcription. This essential signaling pathway is referred to as excitation-transcription (E-T) coupling. Although vascular myocytes can exhibit E-T coupling, the molecular mechanisms and physiological/pathological roles are unknown. Multiscale analysis spanning from single molecules to whole organisms has revealed essential steps in mouse vascular smooth muscle E-T coupling: (1) Upon depolarizing stimulus Ca2+ influx through voltage-dependent Ca2+ channel Cav1.2 activates CaMKK2, which results in phosphorylation of CaMK1a and CREB in the nucleus. (2) Within caveolae the formation of molecular complex of Cav1.2/CaMKK2/CaMK1a is promoted in the vascular myocytes. (3) Ca2+ influx through Cav1.2 localized to caveolae directly activates CaMKK2. (4) CaMK1a is phosphorylated by CaMKK2 at caveolae and translocated to the nucleus upon membrane depolarization. In addition, RNAseq analysis revealed that sustained depolarization of mesenteric artery preparation selectively induced genes related to chemotaxis, leukocyte adhesion and inflammation, and these changes were reversed by inhibitors of Cav1.2, CaMKK2 and CaMK or disruption of caveolae. In the context of pathophysiology, when mesenteric artery was loaded by high pressure in vivo, we noted CREB phosphorylation in myocytes, macrophage accumulation at adventitia, and increased thickness and cross-sectional area of tunica media. These changes were reduced in caveolin1-KO mice or in mice treated with a CaMKK2 inhibitor STO609. In summary, E-T coupling depend on Cav1.2/CaMKK2/CaMK1a localized to caveolae, and this molecular complex converts [Ca2+]i changes to gene transcription, leading to macrophage accumulation and media remodeling for adaptation to increased circumferential stretch.
2022-03-16 | GSE183588 | GEO
Project description:Comparison of the effect of different types of cytosolic Ca2+ elevations (measured by aequorin luminescence) in Arabidopsis seedlings. Calcium elevations are produced by electrical stimulation; namely transient (short, high amplitude) elevation and prolonged (lower amplitude, longer duration)- both were both biologically replicated. Biological replicates were processed as dye-swapped hybridisations.
2010-07-01 | E-MEXP-2661 | biostudies-arrayexpress
Project description:Precise vascular patterning is critical for normal growth and development. The ERG transcription factor drives Delta like ligand 4 (DLL4)/Notch signalling and is thought to act as pivotal regulators of endothelial cell (EC) dynamics and developmental angiogenesis. However, molecular regulation of ERG activity remains obscure. Using a series of EC specific Focal Adhesion Kinase (FAK)-knockout (KO) and point-mutant FAK-knockin mice, we show that loss of ECFAK, its kinase activity or phosphorylation at FAK-Y397, but not FAK-Y861, reduces ERG and DLL4 expression levels together with concomitant aberrations in vascular patterning. Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins identified that endothelial nuclear-FAK interacts with the de-ubiquitinase USP9x and the ubiquitin ligase TRIM25 enzymes. Further in silico analysis corroborates that ERG interacts with USP9x and TRIM25. Moreover, ERG levels are reduced in FAKKO ECs via a ubiquitin-mediated post-translational modification programme involving USP9x and TRIM25. Re-expression of ERG in vivo and in vitro rescues the aberrant vessel sprouting defects observed in the absence of ECFAK. Our findings identify ECFAK as a regulator of retinal vascular patterning by controlling ERG protein degradation via TRIM25/USP9x.
2022-07-05 | PXD033447 | Pride
Project description:The vascular endothelium consists of endothelial cells (ECs) with important biological functions and their impairment is associated with various pathologies. ECs vary based on tissue origin and gene expression, while their functionality depends on calcium (Ca2+) signaling. In tumors, disruption of Ca2+ homeostasis after calcium electroporation (CaEP) has been shown to elicit an enhanced antitumor effect with only minimal effect on normal tissue. The difference in response to CaEP was not only observed between cancer and normal cells, but also between different endothelial cell lines. Although several vascular EC models have been developed, there is a lack of understanding regarding the molecular basis that could help explain different responses of normal tissue to CaEP. Therefore, our study aims to determine the effect of CaEP on established immortalized human EC lines EA.hy926 and HMEC-1 in terms of cytoskeleton, Ca2+ kinetics and differences in gene expression involved in regulation of Ca2+ signaling and homeostasis.
2024-02-21 | GSE244042 | GEO
Project description:Staphylococcus lentus Ca2 genome sequence
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2020-10-28 | GSE115445 | GEO
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