The Schwann Cell as an Active Synaptic Partner

Hyung, Sujin; Jung, Kyuhwan; Cho, Sung Rae; Jeon, Noo Li

doi:10.1002/cphc.201701299

Cited by 9 publications

(6 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Schwann cells provide trophic support and transfer materials to damaged axons via exosomes [95]. Furthermore, they maintain developing synapses, and participate in synaptic pruning [96,97].…”

Section: Nervous System Cells and Tissues: An Overviewmentioning

confidence: 99%

Extracellular Vesicle-Mediated Cell–Cell Communication in the Nervous System: Focus on Neurological Diseases

Bavisotto

Scalia

Gammazza

et al. 2019

IJMS

120

View full text Add to dashboard Cite

Extracellular vesicles (EVs), including exosomes, are membranous particles released by cells into the extracellular space. They are involved in cell differentiation, tissue homeostasis, and organ remodelling in virtually all tissues, including the central nervous system (CNS). They are secreted by a range of cell types and via blood reaching other cells whose functioning they can modify because they transport and deliver active molecules, such as proteins of various types and functions, lipids, DNA, and miRNAs. Since they are relatively easy to isolate, exosomes can be characterized, and their composition elucidated and manipulated by bioengineering techniques. Consequently, exosomes appear as promising theranostics elements, applicable to accurately diagnosing pathological conditions, and assessing prognosis and response to treatment in a variety of disorders. Likewise, the characteristics and manageability of exosomes make them potential candidates for delivering selected molecules, e.g., therapeutic drugs, to specific target tissues. All these possible applications are pertinent to research in neurophysiology, as well as to the study of neurological disorders, including CNS tumors, and autoimmune and neurodegenerative diseases. In this brief review, we discuss what is known about the role and potential future applications of exosomes in the nervous system and its diseases, focusing on cell–cell communication in physiology and pathology.

show abstract

Section: Nervous System Cells and Tissues: An Overviewmentioning

confidence: 99%

Extracellular Vesicle-Mediated Cell–Cell Communication in the Nervous System: Focus on Neurological Diseases

Bavisotto

Scalia

Gammazza

et al. 2019

IJMS

120

View full text Add to dashboard Cite

show abstract

“…To achieve somatic movement, MNs communicate with SCs to coordinate release of neurotransmitters that diffuse across the synaptic cleft and bind cognate receptors on striated muscle (Jones et al, ; Nishimune & Shigemoto, ). Although numerous projects highlight neuron–muscle interactions for motility (Chhabra et al, ; Huie, Almeida, & Ferguson, ; Webster, ), only a handful of NMJ studies use models that include glia to leverage the significant roles of these cells in NMJ function and repair (Brosius Lutz & Barres, ; Du, Chen, Tseng, Eisenberg, & Firestein, ; Hyung, Jung, Cho, & Jeon, ). SC inclusion is vital to regenerative therapies because adult SCs of the peripheral NS possess remarkable regenerative abilities (Jessen & Mirsky, ; Kim, Mindos, & Parkinson, ), including de/differentiation (Arthur‐Farraj et al, ), migration to sites of injury (Ji et al, ; Sohn, Jo, & Park, ), and glial bridging to synapse with adjacent functional neurons (Jones et al, ; Mousavi et al, ).…”

Section: Introductionmentioning

confidence: 99%

Neuronal substrates alter the migratory responses of nonmyelinating Schwann cells to controlled brain‐derived neurotrophic factor gradients

Singh

Robles

Vázquez

2020

J Tissue Eng Regen Med

View full text Add to dashboard Cite

Neurodegeneration and dysfunction cause mobility impairment and/or paralysis in millions of adults, worldwide. Motor deficit and recovery in adults depend upon the plasticity of the neuromuscular junction (NMJ), a tripartite, biochemical synapse that transduces electrical impulses from the brain into voluntary contraction of skeletal muscle. Nonmyelinating Schwann cells (nmSCs) of the NMJ have been increasingly recognized as active synaptic partners with motor neurons and muscle and have become recent therapeutic targets for regeneration. nmSC synaptic transmission, plasticity, and growth are strongly modulated by brain-derived neurotrophic factor (BDNF), whose regenerative abilities have been explored through emerging biomaterials and tissue-engineered systems, as well as via clinical trials. Experimental models engineered to investigate integrated NMJ response(s) to local gradients of BDNF will both advance our understanding of key modulators of synaptic activity, postinjury, and aid in the development of NMJ-targeted, regenerative therapies to restore mobility. The current study examined the ability of nmSCs to respond to microfluidically controlled BDNF signaling upon different haptotactic substrates of motor neurons (MNs) and laminin adhesion coating. Tests seeding nmSCs sequentially with MNs illustrated that sequential seeding reported a fivefold increase in levels of tropomyosin receptor kinase B expression in response to BDNF signaling and a nearly fivefold increase in migration distance along BDNF gradients. By contrast, concurrent seeding of MNs and nmSCs upon laminin adhesion coating illustrated a difference in migration distance of less than one third-fold over control. Our findings are among the first to examine migratory responses of nmSCs for regenerative strategies and highlight the potential to restabilize NMJ synaptic activity by affecting nmSC behaviors through therapeutic BDNF and seeding with MNs.

show abstract

“…tSCs are extremely sensitive to the NMJ status. During nerve retraction, tSCs drastically upregulate several proteins involved in cell structure and cell junctions such as glial fibrillary acidic protein (GFAP), growth-associated protein-43 (GAP-43), low-affinity nerve growth factor (NGF) receptor p75NTR, Nestin, and cell adhesion molecule CD44 among others [22,122]. It has been described that the number of tSC-bridges and nerve-sprouting is regulated by synaptic activity [54,[123][124][125]: tSCs could be detecting the synaptic microenvironment of the NMJ and determining whether to form sprouts toward adjacent NMJs, strongly suggesting the existence of a link between synaptic activity and tSC-mediated repair of the NMJ.…”

Section: Terminal Schwann Cell Agingmentioning

confidence: 99%

Terminal Schwann Cell Aging: Implications for Age-Associated Neuromuscular Dysfunction

Fuertes-Álvarez¹,

Izeta²

2021

Aging and disease

View full text Add to dashboard Cite

Action potential is transmitted to muscle fibers through specialized synaptic interfaces called neuromuscular junctions (NMJs). These structures are capped by terminal Schwann cells (tSCs), which play essential roles during formation and maintenance of the NMJ. tSCs are implicated in the correct communication between nerves and muscles, and in reinnervation upon injury. During aging, loss of muscle mass and strength (sarcopenia and dynapenia) are due, at least in part, to the progressive loss of contacts between muscle fibers and nerves. Despite the important role of tSCs in NMJ function, very little is known on their implication in the NMJ-aging process and in age-associated denervation. This review summarizes the current knowledge about the implication of tSCs in the age-associated degeneration of NMJs. We also speculate on the possible mechanisms underlying the observed phenotypes.

show abstract

The Schwann Cell as an Active Synaptic Partner

Cited by 9 publications

References 58 publications

Extracellular Vesicle-Mediated Cell–Cell Communication in the Nervous System: Focus on Neurological Diseases

Extracellular Vesicle-Mediated Cell–Cell Communication in the Nervous System: Focus on Neurological Diseases

Neuronal substrates alter the migratory responses of nonmyelinating Schwann cells to controlled brain‐derived neurotrophic factor gradients

Terminal Schwann Cell Aging: Implications for Age-Associated Neuromuscular Dysfunction

Contact Info

Product

Resources

About