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TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron

ABSTRACT: TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron

PROVIDER: PRJNA893219 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22013626_1.fastq.gz	Fastqsanger.gz
	SRR22013626_2.fastq.gz	Fastqsanger.gz
	SRR22013627_1.fastq.gz	Fastqsanger.gz
	SRR22013627_2.fastq.gz	Fastqsanger.gz
	SRR22013628_1.fastq.gz	Fastqsanger.gz

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TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (scRNA-Seq)

Project description:TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (scRNA-Seq)

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TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (CRISPR screen)

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TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (CRISPR screen)

Project description:First-in-human clinical trials illustrate the feasibility and translational potential of human pluripotent stem cell (hPSC)-based cell therapy in Parkinson’s disease (PD). However, a major unresolved challenge is the extensive cell death following transplantation with <10% of grafted dopamine neurons surviving. Here, we performed a pooled CRISPR/Cas9 screen to enhance survival of postmitotic dopamine neurons in vivo. We identified TP53-mediated apoptotic cell death as major contributor to dopamine neuron loss and uncovered a causal link of TNFa-NFκB signaling in limiting cell survival. A surface marker screen enabled the purification of midbrain dopamine neurons obviating the need for genetic reporters. Combining cell sorting with adalimumab pretreatment, a clinically approved TNFa inhibitor, enabled efficient engraftment of postmitotic dopamine neurons leading to extensive re-innervation and functional recovery in a preclinical PD mouse model. Thus, transient TNFa inhibition may present a clinically relevant strategy to enhance survival of human PSC-derived lineages in PD and beyond.

2024-04-26 | GSE217131 | GEO

TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (scRNA-Seq)

2024-04-26 | GSE216364 | GEO

TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (RNA-Seq)

Project description:Cas9 screen to enhance survival of postmitotic dopamine neurons in vivo. We identified TP53-mediated apoptotic cell death as major contributor to dopamine neuron loss and uncovered a causal link of TNFa-NFκB signaling in limiting cell survival. A surface marker screen enabled the purification of midbrain dopamine neurons obviating the need for genetic reporters. Combining cell sorting with adalimumab pretreatment, a clinically approved TNFa inhibitor, enabled efficient engraftment of postmitotic dopamine neurons leading to extensive re-innervation and functional recovery in a preclinical PD mouse model. Thus, transient TNFa inhibition may present a clinically relevant strategy to enhance survival of human PSC-derived lineages in PD and beyond.

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TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-26 | GSE216365 | GEO

The expression of inflammatory genes in endothelial cells is inhibited by N-octanoyl dopamine via modulation of the NFkB pathway

Project description:Background: Dopamine has intrinsic receptor-independent anti-inflammatory properties when used at high concentrations. Since cellular uptake of N-octanoyl dopamine (NOD) is far better than of dopamine, NOD might display anti-inflammatory effects already at relative low concentrations. The present study was conducted to assess the anti-inflammatory potential of NOD and to elucidate how this was mediated. Methods: Human umbilical vein endothelial cells (HUVECs) were stimulated with TNF-Î± in the presence of various NOD concentrations. Affymetrix gene expression profiling (GEP), Western blotting, adhesion of peripheral blood mononuclear cells (PBMC) to endothelial cells and NFÎºB activation was studied. Compounds that were structurally related to NOD were used to address the molecular entities within NOD that were required for its anti-inflammatory properties. Results: GEP revealed that NOD down-regulates a wide range of pro-inflammatory mediators. Down-regulation of adhesion molecules was confirmed at the protein level and resulted in a decreased adhesion of PBMC to endothelial cells under static and flow conditions. NOD inhibited NFÎºB independently of IÎºBÎ± degradation. Inhibition was associated with an overall decrease in p65 expression and a significant decrease in p65 phosphorylation at Ser276. De novo protein synthesis was not required for inhibition and was not mediated via HO-1. Redox activity and hydrophobicity of NOD seemed to be important entities for its anti-inflammatory properties. Conclusion: Our data demonstrate that NOD has potent anti-inflammatory effects through its action on NFÎºB. Unlike dopamine, NOD has no adverse effects on blood pressure, making it a promising candidate drug to reduce excessive inflammation occurring under various pathological conditions. A total of 6 different HUVEC lines were used, n=3 for each group (TNF or TNF+ NOD).

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Biphasic activation of WNT signaling enhances the derivation of midbrain dopamine neurons for translational use [RNA-seq]

Project description:We report a novel midbrain dopamine neuron derivation protocol from human pluripotent stem cells (hPSC)s based on a two-step WNT signaling activation strategy. By comparing next-generation sequencing (NGS) derived transcriptome profiling (RNA-seq) of dopamine neuron differentiated cells derived from hPSC with different concentration of Chir-boosting (day4 – day9) measured at day 11 including hPSC, we find that CHIR-boosting improves expression of midbrain markers such as EN1 while minimizing expression of contaminating posterior (hindbrain) and anterior (diencephalic) lineage markers. Furthermore, gene expression analysis from RNA-seq study confirmed the progressive differentiation and maturation of Boost CHIR treated precursors into mDA neurons by day 30 of differentiation. The protocol presented here is the basis for clinical grade dopamine neuron production and preclinical safety and efficacy studies.

2020-12-18 | GSE162883 | GEO

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