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Single-nucleus RNA-seq of human SGs

ABSTRACT: The sympathetic nervous system (SNS) is pivotal in orchestrating the body's response to stress,maintaininghomeostasis, andfacilitatingadaptive physiological changes. The executing neurons responsible for these responses are localized in ganglia, positioned along the sympathetic chain. Here, we performedsingle-nucleussequencingof human sympathetic ganglia from heart healthy specimens obtained at autopsy. Unbiased clustering and trajectory analyses allowed a comprehensive analysis ofthissequencing data, offering valuable insights intoganglionic physiology includinggene expression patterns,cellular composition, intercellular communication as well as cellstatetransitions anddynamics. Strikingly, identifying previously uncharacterized cell types suggests aremarkablyhigher level of complexity than previously appreciated.Our findings highlightthe dynamic and complex physiology of sympathetic ganglia, shedding light on mechanismsgoverning fundamental physiological processes and the intricate interplay of various cell types coordinating the underlying pathways on the transcriptional level. This dataset enhances our knowledge of the SNS and opens avenues for further investigation into its role in health and disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE241386 | GEO | 2023/12/12

REPOSITORIES: GEO

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Sympathetic neuron-associated macrophages contribute to obesity by importing and metabolizing norepinephrine

Project description:The cellular mechanism(s) linking macrophages to norepinephrine (NE)-mediated regulation of thermogenesis has been a topic of debate. Here, we identify sympathetic neuron-associated macrophages (SAMs) as a population of macrophages that mediate clearance of NE via expression of Slc6a2, an NE transporter, and monoamine oxidase A (MAOa), a degradation enzyme. Optogenetic activation of the SNS upregulates NE uptake by SAMs and shifts the SAM profile to a more pro-inflammatory state. NE uptake by SAMs is prevented by genetic depletion of Slc6a2 or inhibition of the transporter. We also found that obesity increases SAM content in the SNS. In two mouse models of obesity, genetic ablation of Slc6a2 in SAMs increases brown adipose tissue (BAT) content, causes browning of white fat, increases thermogenesis and leads to significant and sustained weight loss. We further show that this pathway is conserved as human sympathetic ganglia also contain SAMs and the analogous molecular machinery for NE clearance, thus constituting a potential target for obesity treatment.

2017-10-09 | GSE103847 | GEO

Cell-Type Profiling of the Sympathetic Nervous System Using Spatial Transcriptomics and Spatial Mapping of mRNA [Spatial Transcriptomics]

Project description:Background: The molecular identification of neural progenitor cell populations that connect to establish the sympathetic nervous system (SNS) remains unclear. This is due to technical limitations in the acquisition and spatial mapping of molecular information to tissue architecture. Results: To address this, we applied Slide-seq spatial transcriptomics to intact fresh frozen chick trunk tissue transversely cryo-sectioned at the developmental stage prior to SNS formation. In parallel, we performed age- and location-matched single cell (sc) RNA-seq and 10x Genomics Visium to inform our analysis. Downstream bioinformatic analyses led to the unique molecular identification of neural progenitor cells within the peripheral sympathetic ganglia (SG) and spinal cord preganglionic neurons (PGNs). We then successfully applied the HiPlex RNAscope fluorescence in situ hybridization and multispectral confocal microscopy to visualize 12 gene targets in stage-, age- and location-matched chick trunk tissue sections. Conclusions: Together, these data demonstrate a robust strategy to acquire and integrate single cell and spatial transcriptomic information, resulting in improved resolution of molecular heterogeneities in complex neural tissue architectures. Successful application of this strategy to the developing SNS provides a roadmap for functional studies of neural connectivity and platform to address complex questions in neural development and regeneration.

2023-04-27 | GSE230778 | GEO

Cell-Type Profiling of the Sympathetic Nervous System Using Spatial Transcriptomics and Spatial Mapping of mRNA [Slide-seq]

2023-04-27 | GSE230776 | GEO

Cell-Type Profiling of the Sympathetic Nervous System Using Spatial Transcriptomics and Spatial Mapping of mRNA [RNA-seq]

2023-04-27 | GSE230772 | GEO

Sympathectomy effect on muscle clock

Project description:Characterization of the effect of perturbation of sympathetic nervous system (SNS) on skeletal muscle rhythmic transcriptome.

2024-02-01 | GSE225851 | GEO

Next-generation sequencing facilitates quantitative analysis of T1-T4 sympathetic ganglia transcriptomes from TRKC+/-, AdNTF3-Tg and their respective wild type control mice after 1 day cold exposure at 5℃

Project description:Activation of brown fat thermogenesis increases energy expenditure and alleviates obesity. Sympathetic nervous system (SNS) is important in brown/beige adipocyte thermogenesis. Here we discover a novel fat-derived “adipokine” neurotrophic factor neurotrophin 3 (NTF3) and its receptor Tropomyosin receptor kinase C (TRKC) as key regulators of SNS growth and innervation in adipose tissue. NTF3 is highly expressed in brown/beige adipocytes, and potently stimulates sympathetic neuron neurite growth. NTF3/TRKC regulates a plethora of pathways in neuronal axonal growth and elongation. Adipose tissue sympathetic innervation is significantly increased in mice with adipocyte-specific NTF3 overexpression, but profoundly reduced in mice with TRKC haploinsufficiency (TRKC+/-). Increasing NTF3 via pharmacological or genetic approach promotes beige adipocyte development, enhances cold-induced thermogenesis and protects against diet-induced obesity (DIO); whereas TRKC+/- mice or SNS TRKC deficient mice are cold intolerant and prone to DIO. Thus, NTF3 is an important fat-derived neurotrophic factor regulating SNS innervation, energy metabolism and obesity.

2021-07-15 | GSE173503 | GEO

Loss of adrenergic nerves in bone marrow drives hematopoietic stem cell niche aging

Project description:Aging of hematopoietic stem cells (HSCs) is associated with the decline of their regenerative capacity, and multi-lineage differentiation potential, contributing to development of blood disorders. The bone marrow microenvironment was recently suggested to influence HSC aging, however the underlying mechanisms remain largely unknown. Here, we show that HSC aging critically depends on bone marrow innervation by the sympathetic nervous system (SNS), as premature loss of SNS nerves or adrenoreceptor b3 (ADRb3) signaling in the microenvironment accelerated the appearance of HSC aging phenotypes reminiscent of physiological aging. Strikingly, supplementation of ADRb3 sympathomimetics to old mice significantly rejuvenated in vivo function of old HSCs, suggesting that the preservation or restitution of SNS innervation during aging may hold the potential for novel HSC rejuvenation strategies.

2018-05-01 | GSE109546 | GEO

Sympathetic inputs regulate adaptive thermogenesis in brown adipose tissue through cAMP-Salt inducible kinase axis

Project description:Various physiological stimuli, such as cold environment, diet, and hormones, trigger brown adipose tissue (BAT) to produce heat through sympathetic nervous system (SNS)- and -adrenergic receptors (ARs). The AR stimulation increases intracellular cAMP levels through heterotrimeric G proteins and adenylate cyclases, but the processes by which cAMP modulates brown adipocyte function are not fully understood. Here we described that specific ablation of cAMP production in brown adipocytes led to reduced lipolysis, mitochondrial biogenesis, uncoupling protein 1 (Ucp1) expression, and consequently defective adaptive thermogenesis. Elevated cAMP signaling by sympathetic activation inhibited Salt-inducible kinase 2 (Sik2) through protein kinase A (PKA)-mediated phosphorylation in brown adipose tissue. Inhibition of SIKs enhanced Ucp1 expression in differentiated brown adipocytes and Sik2 knockout mice exhibited enhanced adaptive thermogenesis at thermoneutrality in an Ucp1-dependent manner. Taken together, our data indicate that suppressing Sik2 by PKA-mediated phosphorylation is a requisite for SNS-induced Ucp1 expression and adaptive thermogenesis in BAT, and targeting Sik2 may present a novel therapeutic strategy to ramp up BAT thermogenic activity in humans.

2018-07-12 | PXD009262 | Pride

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