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Transcriptional profiling of monocytes deficient in Nuclear Orphan Receptors NR4A2 and NR4A3 reveals distinct signalling roles related to antigen presentation and viral response.

ABSTRACT: Transcriptional profiling of monocytes deficient in Nuclear Orphan Receptors NR4A2 and NR4A3 reveals distinct signalling roles related to antigen presentation and viral response.

PROVIDER: PRJNA738860 | ENA |

REPOSITORIES: ENA

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Transcriptional profiling of monocytes deficient in Nuclear Orphan Receptors NR4A2 and NR4A3 reveals distinct signalling roles related to antigen presentation and viral response.

Project description:Using RNA-sequencing and strategic bioinformatic analysis we investigated the down-stream effects of NR4A2 and NR4A3 in monocytes and dissected their common and distinct signalling roles.NR4A2 selective genes were most associated with antigen presentation, NR4A3 selective genes were most associated with interferon/viral reponse and NR4A2/3 co-regulated genes were most associated with clasical innate immure response signaling e.g. TLR signaling and chemokine secretion.

2021-06-18 | GSE178391 | GEO

NR4A2 and NR4A3 selectively modulate elements of the monocyte response to buffered hypercapnia

Project description:In wild type, NR4A2-deficient, and NR4A3-deficient monocytes we used RNA-sequencing to investigate the effect of 4hrs of exposure to buffered hypercapnia (10% CO2) compared to normocapnia (5% CO2) with and without the pro-inflammatory stimulus LPS (2.5ug/ml) for the final 2hrs. Buffered hypercapnia causes transcriptional changes associated with altered metabolic function in both the basal and stimulated states.

2024-03-20 | GSE251925 | GEO

The orphan nuclear receptor NR4A3 is involved in the function of dendritic cells

Project description:Transcriptome analysis of LPS-stimulated bone marrow-derived dendritic cells with NR4A3 gene silencing The NR4A3/NOR1 belongs to the NR4A subfamily of the orphan nuclear hormone receptor superfamily, which is activated in a ligand-independent manner. To examine the role of NR4A3/NOR1 in gene expression of dendritic cells (DCs), we introduced NR4A3 siRNA into bone marrow-derived DCs (BMDCs) and determined the expression levels of mRNA and proteins of cytokines, cell surface molecules, NFκB signaling-related proteins, and transcription factors. The expression level of NR4A3 was markedly up-regulated by TLRs-mediated stimulation in DCs. NR4A3 knockdown significantly suppressed LPS, CpG, or poly I:C-mediated up-regulation of CD80, CD86, IL-10, IL-6, and IL-12. Proliferation and IL-2 production levels of T cells co-cultured with NR4A3-knocked down DCs were significantly lower than that of T cells co-cultured with control DCs. Furthermore, the expression of IKKβ, IRF4, and IRF8 was significantly decreased in NR4A3 siRNA-introduced BMDCs. The knockdown experiments using siRNAs for IKKβ, IRF4, and/or IRF8 indicated that LPS-induced up-regulation of IL-10 and IL-6 was reduced in IKKβ knocked down cells, and that the up-regulation of IL-12 was suppressed by the knockdown of IRF4 and IRF8. Taken together, these results indicate that NR4A3 is involved in TLR-mediated activation and gene expression of DCs.

2017-10-01 | GSE101831 | GEO

Transcriptional Profiling of Monocytes Deficient in Nuclear Orphan Receptors <i>NR4A2</i> and <i>NR4A3</i> Reveals Distinct Signalling Roles Related to Antigen Presentation and Viral Response.

Project description: Not available

| S-EPMC8267906 | biostudies-literature

NR4A orphan nuclear receptor family members, NR4A2 and NR4A3, regulate neutrophil number and survival.

Project description: Not available

| S-EPMC5570679 | biostudies-literature

Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3 [ATAC-Seq]

Project description:We analysed the chromatin opening and accessibillity of transcription factor binding motifs of in vitro activated OT-I CD8+ T cells in the absence of NR4A3 to determine the early impact of NR4A3 in CD8 T cell differentiation

2020-08-24 | GSE143511 | GEO

Nkx6.1 regulates islet beta-cell proliferation via Nr4a1 and Nr4a3 nuclear receptors

Project description:Loss of functional beta-cell mass is a hallmark of Type 1 and Type 2 diabetes, and methods for restoring these cells are needed. We have previously reported that overexpression of the homeodomain transcription factor Nkx6.1 in rat pancreatic islets induces beta-cell proliferation and enhances glucose-stimulated insulin secretion, but the pathway by which Nkx6.1 activates beta-cell expansion has not been defined. Here we demonstrate that Nkx6.1 induces expression of the Nr4a1 and Nr4a3 orphan nuclear receptors, and that these factors are both necessary and sufficient for Nkx6.1-mediated beta-cell proliferation. Consistent with this finding, global knockout of Nr4a1 results in a decrease in beta-cell area in neonatal and young mice. Overexpression of Nkx6.1 and the Nr4a receptors results in increased expression of key cell cycle inducers E2F1 and cyclin E1. Furthermore, Nkx6.1 and Nr4a receptors induce components of the anaphase-promoting complex, including Ube2c, resulting in degradation of the cell cycle inhibitor p21CIP1. These studies identify a new bipartite pathway for activation of beta-cell proliferation, suggesting several new targets for expansion of functional beta-cell mass. We set up a microarray using primary rat islets that were left untreated or transduced with adenoviruses overexpressing betagal or Nkx6.1 for 48 h.

2014-02-18 | E-GEOD-55077 | biostudies-arrayexpress

Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3

Project description:Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3

| PRJNA600856 | ENA

NR4A3 plays a pivotal role in the differentiation of monocyte-derived dendritic cells

Project description:The molecular requirements that guide the differentiation of monocytes into macrophages or monocyte-derived dendritic cells (Mo-DCs) are poorly understood. Here, we demonstrate that the nuclear orphan receptor NR4A3 guides monocyte fate and is essential for Mo-DC differentiation. Nr4a3-/- mice are impaired in the in vivo generation of DC-SIGN+ Mo-DCs following LPS stimulation and, as such, are defective at priming a CD8+ T cell response to gram negative bacteria. We also demonstrate that NR4A3 is an essential downstream effector of IRF4 during in vitro differentiation of Mo-DCs with GM-CSF and IL-4 and that, in absence of NR4A3, monocytes are diverted to macrophages. Our transcriptomic analysis of the genes regulated by NR4A3 reveals that the acquisition of the Mo-DC differentiation program is intertwined with the acquisition of a migratory signature. Furthermore, NR4A3 is critical for steady-state migration of non-lymphoid tissue conventional DCs to lymph nodes. Altogether, our results highlight a unique role for NR4A3 in Mo-DC differentiation and in the acquisition of migratory properties.

2019-06-25 | GSE99837 | GEO

Relapse to cocaine-seeking is regulated by medial habenula Nr4a2

Project description:After exposure to drugs of abuse, the reward circuit can experience persistent changes that are thought to underlie relapse behavior. These changes can be epigenetic in nature, and here we identify an epigenetic regulator of memory processes, nuclear orphan receptor subfamily4 groupA member2 (NR4A2 aka NURR1), as necessary for relapse to cocaine-seeking behavior. Nr4a2 is an epigenetically regulated immediate early gene and transcription factor that is highly expressed in the medial habenula (MHb). Despite the well-studied contributions of the MHb to nicotine-associated behaviors, the MHb is not classically included in reward circuits. Therefore, the role of MHb NR4A2 in cocaine-seeking and relapse behavior remains largely unknown. This is a key open question as NR4A2 is a powerful regulator of memory processes dependent on epigenetic mechanisms. In this study, we examined the role of MHb NR4A2 in cued reinstatement of cocaine self-administration in mice, and found that over-expressing a dominant negative form of Nr4a2 (Nurr2c) in the MHb results in a near complete block of relapse-like behavior. We used single-nucleus transcriptomics to characterize the molecular cascade following the manipulation of Nr4a2, revealing changes in transcriptional networks related to addiction, neuroplasticity, and glutamatergic signaling. Together, these results place the MHb in the reward circuit as a pivotal regulator of relapse behavior and demonstrate the importance of NR4A2 as a key mechanism driving relapse behavior in the MHb.

2024-03-01 | GSE208081 | GEO

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