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Human iPSC modeling recapitulates in vivo sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma [Bulk RNA-seq]

ABSTRACT: Human iPSC modeling recapitulates in vivo sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma [Bulk RNA-seq]

PROVIDER: PRJNA871265 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21142700_1.fastq.gz	Fastqsanger.gz
	SRR21142700_2.fastq.gz	Fastqsanger.gz
	SRR21142701_1.fastq.gz	Fastqsanger.gz
	SRR21142701_2.fastq.gz	Fastqsanger.gz
	SRR21142702_1.fastq.gz	Fastqsanger.gz

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Human iPSC modeling recapitulates in vivo sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma

Project description:Human iPSC modeling recapitulates in vivo sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma

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Human iPSC modeling recapitulates in vivo sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma [scRNA-seq]

Project description:Pediatric malignancies, including neuroblastoma, are best understood as disorders of development. Neuroblastoma explicitly represents a failure of sympathoadrenal development. Yet, its molecular pathogenesis remains elusive. The application of an in vitro model of human sympathoadrenal development would allow for studying the normal developmental trajectory. Such a model could also interrogate the early steps toward neuroblastoma transformation utilizing genetic manipulation. However, in vitro models have thus far been unable to generate the cells of interest reliably. We developed and characterized a human in vitro pluripotent stem cell-based model via sequential single-cell RNA sequencing throughout sympathoadrenal development. We demonstrate the power of our model to study early events of the development of human neuroblastoma. We do so by identifying the differences between normal and patient-specific induced pluripotent stem cells, derived from a child with familial neuroblastoma, harboring a germline mutation in the Anaplastic Lymphoma Kinase (ALK) gene.

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Human iPSC modeling recapitulates in vivo sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma [Bulk RNA-seq]

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Human iPSC modeling recapitulates in vivo sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma [scRNA-seq]

Project description:Human iPSC modeling recapitulates in vivo sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma [scRNA-seq]

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Human iPSC modeling recapitulates <i>in vivo</i> sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma.

Project description:Studies defining normal and disrupted human neural crest cell development have been challenging given its early timing and intricacy of development. Consequently, insight into the early disruptive events causing a neural crest related disease such as pediatric cancer neuroblastoma is limited. To overcome this problem, we developed an in vitro differentiation model to recapitulate the normal in vivo developmental process of the sympathoadrenal lineage which gives rise to neuroblastoma. We used human in vitro pluripotent stem cells and single-cell RNA sequencing to recapitulate the molecular events during sympathoadrenal development. We provide a detailed map of dynamically regulated transcriptomes during sympathoblast formation and illustrate the power of this model to study early events of the development of human neuroblastoma, identifying a distinct subpopulation of cell marked by SOX2 expression in developing sympathoblast obtained from patient derived iPSC cells harboring a germline activating mutation in the anaplastic lymphoma kinase (ALK) gene.

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Human iPSC modeling recapitulates in vivo sympathoadrenal development and reveals an aberrant developmental subpopulation in familial neuroblastoma

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

2023-10-16 | GSE211664 | GEO

The Longevity Gene mIndy (I’m Not Dead, Yet) Affects Blood Pressure Through Sympathoadrenal Mechanisms

Project description:Reduced expression of the plasma-membrane citrate-transporter INDY (acronym I’m Not Dead, Yet) extends life span in lower organisms. Deletion of the mammalian Indy (mIndy) gene in rodents improves metabolism via mechanisms akin to caloric restriction, known to lower blood pressure (BP) by sympathoadrenal inhibition. We hypothesized that mIndy deletion attenuates sympathoadrenal support of BP. mINDY-knockout (KO) mice were monitored using radiotelemetry; autonomic cardiovascular control was assessed by pharmacological testing, spectral analysis, urine catecholamines and adrenal transcriptome analysis. In vivo echocardiography, vascular function and steroid hormones were assessed. Continuous arterial BP and heart rate (HR) were reduced in mINDY-KO mice compared to littermate controls. Urinary catecholamines were reduced and the decreases in BP and HR by mIndy deletion were attenuated after autonomic ganglionic blockade. Catecholamine biosynthesis pathways were reduced in mINDY-KO adrenals using unbiased microarray analysis. Citrate, the main mINDY substrate, increased catecholamine content in pheochromocytoma cells, while pharmacological inhibition of citrate uptake blunted the effect. Adrenal size, histological structure and cardiac function were not affected. Our data suggest that deletion of mIndy reduces sympathoadrenal support of BP and HR by attenuating catecholamine biosynthesis. mIndy deletion recapitulates beneficial cardiovascular and metabolic responses to caloric restriction making it an attractive therapeutic target.

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Project description:It is proposed that the impaired sympathoadrenal response to hypoglycemia induced by recurrent insulin-induced hypoglycemia (RH) is an adaptive phenomenon induced by specific changes in microRNA expression in the ventromedial hypothalamus (VMH). To test this hypothesis, genome-wide microRNAomic profiling of the VMH by RNA-sequencing was performed in control and RH treated rats. Differential expression analysis identified microRNA-7a-5p and microRNA-665 as potential mediators of this phenomenon. To further test this hypothesis, experiments were conducted consisting of targeted lentiviral-mediated overexpression of microRNA-7a-5p and downregulation of microRNA-665 in the VMH. Hyperinsulinemic hypoglycemic clamp experiments demonstrated that targeted overexpression of microRNA-7a-5p (but not downregulation of microRNA-665) in the VMH of RH rats restored the epinephrine response to hypoglycemia. This restored response to hypoglycemia was associated with a restoration of GABAA receptor gene expression. Finally, a direct interaction of microRNA-7a-5p with 3’-UTR of GABAA receptor α1-subunit (Gabra1) gene was demonstrated in a luciferase assay. These findings indicate that 1) the impaired sympathoadrenal response induced by RH is associated with changes in VMH microRNA expression, and 2) microRNA-7a-5p, possibly via direct downregulation of GABA receptor gene expression, may serve as a mediator of the altered sympathoadrenal response to hypoglycemia.

2019-10-17 | GSE138472 | GEO

Absence of gut microbial colonization attenuates the sympathoadrenal response to hypoglycemia in mice

Project description:Gut microbiota plays an important role during early development via bidirectional gut- brain signaling. We aimed to explore the potential link between gut microbiota/gut derived metabolites and sympathoadrenal stress responsivity

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