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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

Next Generation Sequencing Facilitates Quantitative Analysis of HCC Cell Line HepG2 Cells with Inhibited P2X7 Receptor Signaling by Antagonist A740003 or A438079

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

2024-11-27 | GSE268508 | 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

Nanobody-based in vivo blockade of the P2X7 ion channel uncovers a hitherto unknown large subpopulation of parenchymal kidney TRM and NKT cells

Project description:The P2X7 ion channel, a key sensor of sterile inflammation, has been implicated as a therapeutic target in glomerulonephritis and P2X7-antagonistic nanobodies can attenuate experimental glomerulonephritis. However, little is known about the expression of P2X7 on renal immune cells. We used i.p. injection of nanobodies in mice followed by flow cytometry analysis of parenchymal T cells and RNA-sequencing to elucidate the expression and function of P2X7 on parenchymal and vascular immune cells in the mouse kidney. We show that parenchymal T cells, including a large subset NKT cells and tissue-resident memory T cells, display much higher cell surface levels of P2X7 than vascular T cells. These parenchymal T cells are highly sensitive to NAD+-induced cell death unless injection of P2X7-antagonistic nanobodies was performed before cell preparation. Remarkably, within 30 min after a single intraperitoneal injection of P2X7-blocking nanobodies, P2X7 is fully occupied by the injected nanobodies on parenchymal T cells in the kidney. This results in an effective protection of these cells from NAD+-induced cell death. Conversely, systemic injection of NAD+ that mimics sterile inflammation results in the selective depletion of P2X7hiCD69hi T cells from the kidney parenchyma. In summary, our study uncovers a novel purinergic regulatory mechanism affecting kidney resident T cell populations.

2024-12-04 | GSE241191 | GEO

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