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Adeno-associated virus (AAV) 9-mediated gene delivery of Nurr1 and Foxa2 cures symptoms and pathologies of Alzheimer disease model mice by suppressing neuro-inflammation and glial pathology.

ABSTRACT: Adeno-associated virus (AAV) 9-mediated gene delivery of Nurr1 and Foxa2 cures symptoms and pathologies of Alzheimer disease model mice by suppressing neuro-inflammation and glial pathology.

PROVIDER: PRJNA828425 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18829381_1.fastq.gz	Fastqsanger.gz
	SRR18829381_2.fastq.gz	Fastqsanger.gz
	SRR18829382_1.fastq.gz	Fastqsanger.gz
	SRR18829382_2.fastq.gz	Fastqsanger.gz
	SRR18829383_1.fastq.gz	Fastqsanger.gz

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Adeno-associated virus (AAV) 9-mediated gene delivery of Nurr1 and Foxa2 cures symptoms and pathologies of Alzheimer disease model mice by suppressing neuro-inflammation and glial pathology.

Project description:In this study, AAV9-Nurr1 and AAV9-Foxa2 (or AAV9-Control as sham-operated control) were injected to hippocampus of 15-18 months old 3xTg Alzheimer's disease mice. And mouse hippocampal glia were primarily cultured at postnatal day 1 and forced expression of Nurr1 and Foxa2 with lentivirus (or lenti-Control).

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Microarray analysis of Nurr1 and Foxa2 synergisitic effect for DA neuron induction

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Microarray analysis of Nurr1 and Foxa2 synergisitic effect for DA neuron induction

Project description:Analysis of dopaminergic neuronal gene expression changes by Nurr1 and/or Foxa2 overexpression. Result provides that Foxa2 potentiates Nurr1-induced DA neuronal phenotype gene expression. To identify the syergism of Nurr1 and Foxa2 for developing DA neural precursors, neural precusor cells (NPCs) isolated from embryonic brain were treated control, Nurr1, Foxa2 and Nurr1-Foxa2 retrovirus. After treatment of retroviruses, NPCs were cultrued in N2 media withdrawn mitogen (bFGF, EGF) for differetiation of DA neuron. Total RNA was obtained from NPCs in differentiation day 2.

2014-01-16 | E-GEOD-54086 | biostudies-arrayexpress

Identification of genes modulated by Nurr1 overexpression

Project description:Identification of genes modulated by Nurr1 overexpression in HB-1 HB-1 cells overexpressing Nurr1

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NURR1 activation in skeletal muscle controls systemic energy homeostasis (ChIP-seq)

Project description:Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1 and transgenic overexpression of NURR1 in skeletal muscle confers an endurance phenotype in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.

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NURR1 activation in skeletal muscle controls systemic energy homeostasis (RNA-seq)

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Project description:Effects of Nurr1 silencing and treatment with Nurr1 ligand Simvastatin in presence or absence of LPS-stimulus on gene expression in human astrocytes (T98G).

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Comparison of neural stem cell lines overexpressing Nurr1 to clonal controls

Project description:The orphan nuclear receptor Nurr1 has been shown to be critical for the development of ventral midbrain dopaminergic neurons. Consequently, the development of ES cells overexpressing Nurr1 has raised hope for the development of cell replacement therapies for Parkinson's Disease to replace degenerated dopaminergic neurons. However, the molecular consequences of Nurr1 on gene expression in these cells remain unknown. To address this, stable, clonal, c17.2 neural stem cell lines were established that overexpressed the orphan nuclear receptor Nurr1 (clone 42 & clone 48) or parental control cell line (puroB & puroD, respectively). Keywords: genetic modification

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The transcription factor nurr1 exerts concentration-dependent effects on target genes mediating distinct biological processes

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