Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1033983 | ENA |
REPOSITORIES: ENA
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Project description:Decoding muscle-resident Schwann cell dynamics during neuromuscular junction remodeling [scRNA-seq]
| PRJNA1369203 | ENA
Project description:Decoding muscle-resident Schwann cell dynamics during neuromuscular junction remodeling [spinal crush]
| PRJNA1233797 | ENA
Project description:This investigation leverages single-cell RNA sequencing (scRNA-Seq) to delineate the contributions of muscle-resident Schwann cells to neuromuscular junction (NMJ) remodeling in models of healthy, partially denervated, and completely denervated muscles. The study identifies several distinct Schwann cell subtypes, notably a novel terminal Schwann cell (tSC) subtype integral to the denervation-reinnervation cycle, distinguished by a transcriptomic signature indicative of cell migration and polarization. It also characterizes three myelin Schwann cell subtypes, which are notably enriched with genes associated with myelin production, in addition to mesenchymal differentiation and collagen synthesis. Importantly, SPP1 signaling emerges as a pivotal regulator of NMJ dynamics, promoting Schwann cell proliferation and muscle reinnervation across the studied nerve injury models. These findings advance our understanding of NMJ maintenance and regeneration and underscore the therapeutic potential of targeting specific molecular pathways to treat neuromuscular and neurodegenerative disorders.
2025-03-12 | GSE291457 | GEO
Project description:Understanding neuromuscular junction (NMJ) repair mechanisms is essential for addressing degenerative neuromuscular conditions. Here, we focus on the role of muscle-resident Schwann cells in NMJ reinnervation. Using an accepted model of progressive NMJ degeneration, Sod1-/- mice, we identified a clear NMJ ‘regenerative window’ that allowed us to define cellular and molecular regulators of synapse remodeling and muscle fiber reinnervation. High-resolution imaging and single-cell RNA sequencing provide a detailed analysis of Schwann cell number, morphology, and transcriptome revealing multiple subtypes, including a previously unrecognized terminal Schwann cell (tSC) population expressing a synapse promoting signature. We also discovered a novel SPP1-driven cellular interaction between myelin Schwann cells and tSCs and show that it promotes tSC proliferation and reinnervation following nerve injury in wild type mice. Our findings offer important insights into molecular regulators critical in NMJ reinnervation that are mediated through tSCs to maintain NMJ function.
2024-11-02 | GSE246865 | GEO
Project description:Understanding neuromuscular junction (NMJ) repair mechanisms is essential for addressing degenerative neuromuscular conditions. Here, we focus on the role of muscle-resident Schwann cells in NMJ reinnervation. Using an accepted model of progressive NMJ degeneration, Sod1-/- mice, we identified a clear NMJ regenerative window that allowed us to define cellular and molecular regulators of synapse remodeling and muscle fiber reinnervation. High-resolution imaging and single-cell RNA sequencing provide a detailed analysis of Schwann cell number, morphology, and transcriptome revealing multiple subtypes, including a previously unrecognized terminal Schwann cell (tSC) population expressing a synapse promoting signature. We also discovered a novel SPP1-driven cellular interaction between myelin Schwann cells and tSCs and show that it promotes tSC proliferation and reinnervation following nerve injury in wild type mice. Our findings offer important insights into molecular regulators critical in NMJ reinnervation that are mediated through tSCs to maintain NMJ function.
2025-12-09 | GSE311353 | GEO
Project description:The molecular mechanisms underlying the opposing states of muscle atrophy (such as with disuse or in aging) and hypertrophy (such as with increased physical activity) are still not well-defined. Progress has been slowed by challenges in characterizing the niche heterogeneity of skeletal muscle (whereby myofibers are the most abundant) and in obtaining well-characterized samples. Here we describe: i) changes in muscle cell populations that are undergoing atrophy or hypertrophy, with complex, opposing cell transcriptional responses during each process; and ii) a remarkable remodeling of the neuromuscular junction (NMJ) domain, whereby we identify emerging new subpopulations of synaptic myonuclei (SynM) and terminal Schwann cells (tSCs) that are specifically adapted to each growth/atrophy condition. High-resolution 3D imaging and spatial transcriptomics reveal these structural and molecular adaptations at the tissue level. Critically, these changes also occur in the NMJ of both denervated and exercised human muscle. Our study lays the ground for identifying novel targets for medical, pharmacological and lifestyle interventions in aging and disease.
2026-04-23 | GSE294765 | GEO
Project description:The molecular mechanisms that govern muscle hypertrophy (as induced by increased physical activity) remain incompletely defined. Through RNA-seq of human muscle, we confirm observations from mice that extensive remodeling of the neuromuscular junction (NMJ) occurs in human muscle after exercise.
2026-04-23 | GSE312393 | GEO
Project description:The molecular mechanisms that govern muscle atrophy (as seen in disuse or aging) remain incompletely defined. Through RNA-seq of human muscle, we confirm observations from mice that extensive remodeling of the neuromuscular junction (NMJ) occurs in human denervated muscle.
2026-04-23 | GSE311567 | GEO
Project description:Neuromuscular networks assemble during early human embryonic development and are essential for the control of body movement. Previous neuromuscular junction modeling efforts using human pluripotent stem cells (hPSCs) generated either spinal cord neurons or skeletal muscles in monolayer culture. Here, we use hPSC-derived axial stem cells, the building blocks of the posterior body, to simultaneously generate spinal cord neurons and skeletal muscle cells that self-organize to generate human neuromuscular organoids (NMOs) that can be maintained in 3D for several months. Single-cell RNA-sequencing of individual organoids revealed reproducibility across experiments and enabled the tracking of the neural and mesodermal differentiation trajectories as organoids developed and matured. NMOs contain functional neuromuscular junctions supported by terminal Schwann cells. They contract and develop central pattern generator-like neuronal circuits. Finally, we successfully use NMOs to recapitulate key aspects of myasthenia gravis pathology, thus highlighting the significant potential of NMOs for modeling neuromuscular diseases in the future.
2020-01-20 | GSE128357 | GEO