The role of somatosensory innervation of adipose tissues
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA856651 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20019843.fastq.gz | Fastqsanger.gz | |||
| SRR20019844.fastq.gz | Fastqsanger.gz | |||
| SRR20019845.fastq.gz | Fastqsanger.gz | |||
| SRR20019846.fastq.gz | Fastqsanger.gz | |||
| SRR20019847.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the role of somatosensory innervation of adipose tissues, we unilaterally ablate sensory innervation of adipose tissues, and profiled the gene expression in the inguinal adipose tissues 4 weeks after sensory ablation surgery.
2022-07-10 | GSE207664 | GEO
Project description:Compared to the well-established functions of sympathetic innervation, the role of sensory afferents in adipose tissues remains less understood. Recent work revealed the anatomical and physiological significance of adipose sensory innervation; however, its molecular underpinning remains unclear. Here, using organ-targeted single-cell RNA sequencing, we identified the mechanoreceptor PIEZO2 as one of the most prevalent receptors in fat-innervating dorsal root ganglia (DRG) neurons. Selective PIEZO2 deletion in fat-innervating neurons led to molecular alternations in adipose tissue similar to DRG ablation. Conversely, a gain-of-function PIEZO2 mutant shifted the adipose phenotypes in the opposite direction. These results indicate that PIEZO2 plays a major role in the sensory regulation of adipose tissues. This discovery opens new avenues for exploring mechanosensation in organs not traditionally considered mechanically active, such as the adipose tissues, and therefore sheds light on the broader significance of mechanosensation in regulating organ function and homeostasis.
2025-02-02 | GSE286425 | GEO
Project description:Compared to the well-established functions of sympathetic innervation, the role of sensory afferents in adipose tissues remains less understood. Recent work revealed the anatomical and physiological significance of adipose sensory innervation; however, its molecular underpinning remains unclear. Here, using organ-targeted single-cell RNA sequencing, we identified the mechanoreceptor PIEZO2 as one of the most prevalent receptors in fat-innervating dorsal root ganglia (DRG) neurons. Selective PIEZO2 deletion in fat-innervating neurons led to molecular alternations in adipose tissue similar to DRG ablation. Conversely, a gain-of-function PIEZO2 mutant shifted the adipose phenotypes in the opposite direction. These results indicate that PIEZO2 plays a major role in the sensory regulation of adipose tissues. This discovery opens new avenues for exploring mechanosensation in organs not traditionally considered mechanically active, such as the adipose tissues, and therefore sheds light on the broader significance of mechanosensation in regulating organ function and homeostasis.
2025-02-02 | GSE286424 | GEO
Project description:A key role of PIEZO2 mechanosensitive ion channel in adipose sensory innervation [scRNA-seq]
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Project description:The sympathetic nervous system innervates peripheral organs to regulate their function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promote sympathetic innervation1,2. The molecular basis of this bi-directional communication is unknown. Here we use thermogenic adipose tissue from mice as a model system to show that T cells, specifically T cells, have a crucial role in promoting sympathetic innervation, at least in part by driving the expression of TGF1 in parenchymal cells via the IL-17 receptor complex (IL-17RC). Ablation of IL-17RC specifically in adipose tissue reduces expression of TGF1 in adipocytes, impairs local sympathetic innervation and causes obesity and other metabolic phenotypes that are consistent with defective thermogenesis; innervation can be fully rescued by restoring TGF1 expression. Ablating cells and the IL-17RC signalling pathway also impairs sympathetic innervation in salivary glands and the lungs. These findings demonstrate coordination between T cells and parenchymal cells to regulate sympathetic innervation.
2020-03-02 | PXD017424 | Pride
Project description:A key role of PIEZO2 mechanosensitive ion channel in adipose sensory innervation [bulk RNA-seq]
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Project description:Brown Adipose Tissue (BAT) is driven by neural innervation for thermogenesis and represents a potential therapeutic target for human obesity. However, the regulation mechanisms of BAT's neural innervation are still unclear. In this study, we validate the terminal regulation mechanism of BAT's neural innervation in which Schwann cells (SCs) control the neural innervation and remodeling of BAT by regulating the distribution of nerve endings. We found that specific ablation of Olfm4 in brown adipocytes instigates an abnormal dedifferentiation and atrophy of mature SCs, which is mediated by the activation of the MEK/ERK signaling axis. This atrophy results in a decrease in the distribution of myelinated sensory and unmyelinated sympathetic nerve endings, leading to a reduction in BAT's neural innervation and thermogenic impairment. Consequently, mice exhibit heightened sensitivity to cold and diet-induced obesity. Notably, the application of a MEK/ERK inhibitor reverses this abnormal dedifferentiation of SCs, rescuing these phenotypes. In addition, our study describes the profound remodeling process that SCs undergo in response to temperature changes, wherein SCs experience reversible dedifferentiation in response to thermal neutrality or mild cold exposure, thus modulating the remodeling of the BAT neural network. Importantly, inhibition of MEK/ERK blocks this dedifferentiation of SCs, reversing thermal neutrality-induced BAT remodeling, thereby reinforcing the central role of SCs in the complex cellular response during temperature-induced BAT remodeling. In conclusion, our study confirms the crucial regulatory role of SCs in the neural innervation and remodeling process of BAT, offering novel insights for the activation of BAT to treat obesity.
2023-10-15 | GSE243317 | GEO
Project description:The sympathetic nervous system innervates peripheral organs to regulate their function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promote sympathetic innervation. The molecular basis of this bi-directional communication remains to be fully elucidated. We use thermogenic adipose tissue as a model system to show that T cells, specifically gdT cells, play a critical role in promoting sympathetic innervation, at least in part through driving TGFβ1 expression in parenchymal cells via IL-17 Receptor C. Adipose-specific ablation of IL-17 Receptor C reduces TGFβ1 expression in adipocytes, impairs local sympathetic innervation and causes obesity and other metabolic phenotypes consistent with defective thermogenesis; innervation can be fully rescued by restoring TGFβ1 expression. Ablating gdT cells and the IL-17 Receptor C signaling pathway also impairs sympathetic innervation in salivary glands and the lung. These findings demonstrate T cell/parenchymal cell coordination to regulate sympathetic innervation.
2020-02-28 | GSE144255 | GEO
Project description:Tissue resident macrophages provide a systemic innate immune defense network and critically contribute to establishment and maintenance of tissue homeostasis. Here we used constitutive and inducible mutagenesis to delete the nuclear transcription regulator methyl-CpG binding protein 2 (MeCP2) in defined tissue macrophages. Animals lacking the Rett syndrome-associated gene in macrophages did not show signs of neurodevelopmental disorder, but surprisingly displayed altered body composition and spontaneous obesity. This phenotype involved neither hyper-phagia, primary hyper-insulinemia nor inflammation, but rather could be linked to impaired brown adipose tissue (BAT) function. Specifically, mutagenesis of a BAT-resident CX3CR1+ macrophage subpopulation compromised homeostatic, though not acute cold-induced thermogenesis. Mechanistically, steady state BAT malfunction of pre-obese mice harboring mutant macrophages was associated with decreased sympathetic innervation and lower local norepinephrine titers, resulting in reduced adipocyte expression of the thermogenic factors UCP1 and DIO2. Mutant macrophages were found to over-express PlexinA4, which might contribute to the phenotype by repulsion of Sema6A-expressing sympathetic axons. Collectively, we report a previously unappreciated homeostatic role of macrophages in the control of tissue innervation, disruption of which in BAT results in metabolic imbalance.
2017-05-01 | GSE95859 | GEO
Project description:FoxO1 is a transcription factor known to regulate metabolism and functions of different tissues. To study the role of FoxO1 in adipose biology, this study examined the transcript profile in inguinal and gonadal adipose tissues from conditional adipose FoxO1 knockout mice and floxed FoxO1 (control) mice.
2024-10-01 | GSE227591 | GEO