Mus musculus
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ABSTRACT:
PROVIDER: PRJNA395644 | ENA |
REPOSITORIES: ENA
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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
Project description:Nuclear orphan receptor TLX affects gene expression in pancreatic beta cells
| PRJNA277312 | ENA
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
Project description:Neural crest cells are migratory progenitor cells that contribute to nearly all tissues and organs throughout the body. Their formation, migration and differentiation are regulated by a multitude of signaling pathways, that when disrupted can lead to disorders termed neurocristopathies. While work in avian and amphibian species has revealed essential factors governing the specification and induction of neural crest cells during gastrulation and neurulation in non-mammalian species, their functions do not appear to be conserved in mice, leaving major gaps in our understanding of neural crest cell formation in mammals. Here we describe Germ Cell Nuclear Factor (GCNF/Nr6a1), an orphan nuclear receptor, as a critical regulator of neural crest cell formation in mice. Gcnf null mutant mice, exhibit a major disruption of neural crest cell formation. The purpose of this experiment is to examine gene expression changes in response to Gcnf mutation in E9.0 mouse embryos.
2022-02-01 | GSE166458 | GEO
Project description:The orphan nuclear hormone receptor ERRβ controls rod photoreceptor survival.
| PRJNA127231 | ENA
Project description:Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3
| PRJNA600856 | ENA
Project description:Orphan Nuclear Receptor ERRγ is required for pancreatic islet beta-cell maturation
| PRJNA242357 | ENA
Project description:Medial arterial calcification is a chronic systemic vascular disorder distinct from atherosclerosis and is commonly observed in patients with chronic kidney disease (CKD), diabetes mellitus, and aging individuals. We previously showed that orphan nuclear receptor NR4A3 is a key regulator in the progression of apolipoprotein (apo) A-IV-induced atherosclerosis; however, little is known about its role in vascular calcification. NR4A3 expression was upregulated in calcified aortic tissues from CKD mice or 1,25(OH)2VitD3 overload-induced mice, and in human calcified aorta. NR4A3 deficiency preserved VSMCs contractile phenotype, inhibited the expression of osteoblast differentiation-related genes, and reduced calcium deposition in the vasculature.
2024-05-14 | GSE254077 | GEO
Project description:Medial arterial calcification is a chronic systemic vascular disorder distinct from atherosclerosis and is commonly observed in patients with chronic kidney disease (CKD), diabetes mellitus, and aging individuals. We previously showed that orphan nuclear receptor NR4A3 is a key regulator in the progression of apolipoprotein (apo) A-IV-induced atherosclerosis; however, little is known about its role in vascular calcification. NR4A3 expression was upregulated in calcified aortic tissues from CKD mice or 1,25(OH)2VitD3 overload-induced mice, and in human calcified aorta. NR4A3 deficiency preserved VSMCs contractile phenotype, inhibited the expression of osteoblast differentiation-related genes, and reduced calcium deposition in the vasculature.
2024-05-14 | GSE254076 | GEO
Project description:Medial arterial calcification is a chronic systemic vascular disorder distinct from atherosclerosis and is commonly observed in patients with chronic kidney disease (CKD), diabetes mellitus, and aging individuals. We previously showed that orphan nuclear receptor NR4A3 is a key regulator in the progression of apolipoprotein (apo) A-IV-induced atherosclerosis; however, little is known about its role in vascular calcification. NR4A3 expression was upregulated in calcified aortic tissues from CKD mice or 1,25(OH)2VitD3 overload-induced mice, and in human calcified aorta. NR4A3 deficiency preserved VSMCs contractile phenotype, inhibited the expression of osteoblast differentiation-related genes, and reduced calcium deposition in the vasculature.
2024-05-14 | GSE254075 | GEO