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Genetic deletion of P2X7 receptors causes genome-wide alteration of gene expression and results in antidepressant phenotype in mice amygdale

ABSTRACT: The purpose of the study was to explore the role of P2X7 receptors (P2X7R) in mood related behavior we have employed whole genome microarray expression profiling as a discovery platform.To identify genes affected by the genetic deletion of P2X7 receptors in the mouse amygdala we performed gene expression microarray analysis. For validation of differentially expressed genes, we performed TaqMan real-time RT-PCR.Our microarray studies have identified 7217 transcripts that were significantly affected by the deficiency of P2X7 receptor. Validation experiments revealed that among these genes at least 30 genes could be associated to synaptic signaling, neuroplasticity and thereby to the pathogenesis of depression (e.g. beta and gamma subunits of GABAA receptor, ionotropic glutamate receptors, α2 adrenergic receptor, which were down regulated in KO mice). 287 transcripts were found be more than two-fold over-expressed in the LPS treated groups which can be classified according to their inflammatory biological function: Il4ra, Saa1, chemokine ligands.

ORGANISM(S): Mus musculus

PROVIDER: GSE21218 | GEO | 2011/03/31

SECONDARY ACCESSION(S): PRJNA126529

REPOSITORIES: GEO

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Genetic deletion of P2X7 receptors causes genome-wide alteration of gene expression and results in antidepressant phenotype in mice amygdale

Project description:The purpose of the study was to explore the role of P2X7 receptors (P2X7R) in mood related behavior we have employed whole genome microarray expression profiling as a discovery platform.To identify genes affected by the genetic deletion of P2X7 receptors in the mouse amygdala we performed gene expression microarray analysis. For validation of differentially expressed genes, we performed TaqMan real-time RT-PCR.Our microarray studies have identified 7217 transcripts that were significantly affected by the deficiency of P2X7 receptor. Validation experiments revealed that among these genes at least 30 genes could be associated to synaptic signaling, neuroplasticity and thereby to the pathogenesis of depression (e.g. beta and gamma subunits of GABAA receptor, ionotropic glutamate receptors, M-NM-12 adrenergic receptor, which were down regulated in KO mice). 287 transcripts were found be more than two-fold over-expressed in the LPS treated groups which can be classified according to their inflammatory biological function: Il4ra, Saa1, chemokine ligands. Intraperitoneal injection of LPS induced alteration of gene expression in mouse amygdala was measured at 6 hours after exposure to doses of 250M-BM-5g/kg. Four independent experiments were performed for each of the four experimental groups (wild type mice and P2X7R -/- KO and saline treatment and LPS treatment).

2011-03-31 | E-GEOD-21218 | biostudies-arrayexpress

P2X7 receptor-dependent microRNA expression profile in the brain following status epilepticus in mice

Project description:We explored the microRNA expression profile in mice lacking the P2X7 receptor before and after seizures. Genome-wide microRNA profiling was performed using hippocampi from wild-type and P2X7 knock-out mice following status epilepticus induced by intraamygdala kainic acid. This revealed that genetic deletion of the P2X7 receptor results in distinct patterns of microRNA expression. Specifically, we found that in vehicle-injected control mice the lack of P2X7 resulted in the up-regulation of 50 microRNAs and down-regulation of 35 microRNAs. Post-status epilepticus, P2X7 deficiency let to the up-regulation of 44 microRNAs while 13 microRNAs were down-regulated. Moreover, there was only limited overlap between identified P2X7-dependent microRNAs between control conditions and post-status epilepticus, suggesting P2X7 regulating the expression of different microRNAs during normal physiology and pathology. Bioinformatics analysis found that genes targeted via P2X7-dependent microRNAs were particularly overrepresented within pathways involved in intracellular signalling, inflammation and cell death, processes repeatedly linked to P2X7. Moreover, whereas genes involved in signalling pathways and inflammation were common among up-and down-regulated P2X7-dependent miRNAs during physiological and pathological conditions, genes associated with cell death seemed to be restricted to up-regulated miRNAs during both physiological conditions and post-status epilepticus. Taken together, our results demonstrate that P2X7 impacts on the expression profile of microRNAs in the brain, thereby possibly contributing to both the maintenance of normal cellular homeostasis and pathological processes.

2020-06-25 | GSE153204 | GEO

The ATP-P2X7 signaling axis is dispensable for obesity-associated inflammasome activation in adipose tissue

Project description:Inflammasome activation in adipose tissue has been implicated in obesity-associated insulin resistance and type 2 diabetes. However, when and how inflammasome is activated in adipose tissue remains speculative. Here we test the hypothesis that extracellular ATP, a potent stimulus of inflammasome in macrophages via purinergic receptor P2X, ligand-gated ion channel, 7 (P2X7), may play a role in inflammasome activation in adipose tissue in obesity. Our data show that inflammasome is activated in adipose tissue upon 8-week feeding of 60% HFD, coinciding with the onset of hyperglycemia and hyperinsulinemia as well as the induction of P2X7 in adipose tissue. Unexpectedly, P2X7-deficient animals on HFD exhibit no changes in metabolic phenotypes, nor in inflammatory responses or inflammasome activation when compared to the wildtype controls. Similar observations have been obtained in hematopoietic cell-specific P2X7-deficient animals generated by bone marrow transplantation. Thus, we conclude that inflammasome activation in adipose tissue in obesity coincides with the onset of hyperglycemia and hyperinsulinemia, but unexpectedly, is not mediated by the ATP-P2X7 signaling axis. The nature of the inflammasome-activating danger signal(s) in adipose tissue in obesity remains to be characterized. Wild type and P2X7 knockout mice were fed a low fat diet (chow) or high fat diet for 12 weeks. After the diet intervention period, the animals were killed and epididymal white adipose tissue was removed. Total RNA was isolated and subjected to gene expression profiling.

2012-02-24 | E-GEOD-36033 | biostudies-arrayexpress

Gene expression profile of Wild Type (WT) and P2x7 knockout (P2X7-KO) leukemia leukemia-initiating cells Transcriptomes

Project description:To determine the underlying molecular mechanisms that control the homing and self-renewal activities of P2x7-null Mac-1+c-Kit+ LICs, WT and P2x7-null LICs were WT and P2x7-KO were sorted by flow cytometry, followed by the extraction of total RNA and subjected to the RNA-sequencing.

2023-11-30 | GSE162468 | GEO

Retrieval of inflammation-compromised periodontal ligament stem cells from dysfunction by exosomes derived from P2X7 receptor gene-modified cells

Project description:Exosomes derived from P2X7 gene modified stem cells could enhance the osteogenic differentiation of periodontal ligament stem cells under inflammatory cultural conditions. In order to identify differentially expressed miRNAs between Exs-Ad-P2X7 and Exs-Ad- control, total RNA from exosomes were extracted by TRIzol™ Reagent (Invitrogen) according to the instructions. Then, miRNA profile of Exs-Ad-P2X7 and Exs-Ad-control form 3 different individuals were sequenced by Agilent miRNA Microarray System and further confirmed by real-time PCR.

2020-10-28 | GSE140356 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of DLBCL Cell Line SU-DHL-4 Cells with P2X7 Receptor Signaling Activation or Inhibition

Project description:The goals of this study aim to reveal the role of P2X7 receptor signaling in DLBCL

2023-07-12 | GSE225174 | GEO

The ATP-P2X7 signaling axis is dispensable for obesity-associated inflammasome activation in adipose tissue

2012-02-24 | GSE36033 | GEO

Gene expression changes in wide-type P2X7 overexpressed MLL-AF9 induced mouse acute myeloid leukemia (AML)

Project description:P2X7 was significantly up-regulated in leukemia patients, especially in AML (MLL-AF9) and often related to poor prognosis.We compared the transcriptomic changes in MLL-AF9 induced mouse AML and overexpressed wP2X7 in MLL-AF9 induced AML. Engaged to explore the mechanism of P2X7 in leukemia progression. Mouse AML was induced by expressing MLL-AF9 in mouse HSPCs. Leukemia cells were divided into two groups, c-kit+ and c-kit-. Due to leukemia cells were nearly 95% c-kit+ in P2X7-overexpressed AML cells, we set up four groups of leukemia cells, namely leukemia total cells (V total), leukemia c-kit positive cells (V c-kit+), leukemia c-kit negative cells (V c-kit-), overexpressed wide type P2X7 leukemia cells (wP2X7).

2021-12-29 | GSE92969 | GEO

Secretome of P2X7 receptor - Macrophage activation and polarization modify P2X7 receptor secretome influencing the inflammatory process

Project description:In order to determine P2X7R secretome we analyzed the proteins present in cell-free supernatants from wild-type (P2rx7+/+) or P2rx7-/- bone marrow-derived macrophages (BMDMs) polarized either to M1 or M2 and subsequently treated with ATP. BMDMs were primed with LPS (M1) or IL-4 (M2) for 4 hours and the proteins secreted during this step were extensively washed with PBS before ATP was added in fresh buffer. The complex mixture of proteins obtained in the macrophages supernatants after ATP stimulation were fractionated using one dimension gel electrophoresis and 10 bands were selected for LC-MS/MS analysis based in their presence in higher intensity in P2rx7+/+ supernatant compared with P2rx7-/- supernatant.

2016-03-11 | PXD001981 | Pride

p53-Dependent Induction of P2X7 on Hematopoietic Stem and Progenitor Cells Regulates Hematopoietic Response to Genotoxic Stress [ChIP-seq]

Project description:Stem and progenitor cells are the main mediators of tissue renewal and repair, both under homeostatic conditions and in the response to physiological stress and injury. Hematopoietic system is responsible for the regeneration of blood and immune cells, and is maintained by bone marrow resident hematopoietic stem and progenitor cells (HSPCs). Hematopoietic system is particularly susceptible to injury in response to genotoxic stress, resulting in risk of bone marrow failure and secondary malignancies in cancer patients undergoing radiotherapy. Here we analyze the in vivo transcriptional response of HSPCs to genotoxic stress in a mouse whole body irradiation model, and together with p53 ChIP-Seq and studies in p53-knockout (p53KO) mice, characterize the p53-dependent and p53-independent branches of this transcriptional response. Our work demonstrates the p53-independent induction of inflammatory transcriptional signatures in HSPCs in response to genotoxic stress, and identifies multiple novel p53-target genes induced in HSPCs in response to whole body irradiation. In particular, we establish the direct p53-mediated induction of P2X7 expression on HSCs and HSPCs in response to genotoxic stress. We further demonstrate the role of P2X7 in hematopoietic response to acute genotoxic stress, with P2X7-deficiency significantly extending mouse survival in irradiation-induced hematopoietic failure. We also demonstrate the role of P2X7 in the context of long-term HSC regenerative fitness following sublethal irradiation. Overall our studies provide important insights into the mechanisms of HSC response to genotoxic stress and further suggests P2X7 as a target for pharmacological modulation of HSC fitness and hematopoietic response to genotoxic injury.

2021-10-09 | GSE171694 | GEO

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