Molecular mechanisms in schwann cell survival and death during peripheral nerve development, injury and disease

2005 ◽  
Vol 7 (1-2) ◽  
pp. 151-167 ◽  
Author(s):  
Kristy Boyle ◽  
Michael F. Azari ◽  
Christos Profyris ◽  
Steven Petratos
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Cell Survival ◽  
Molecular Mechanisms ◽  
Nerve Development

Galectin-3 is differentially expressed during peripheral nerve development: Dependence on the Schwann cell phenotype

2002 ◽  
Vol 30 (2) ◽  
pp. 71-82 ◽  
Author(s):  
Penka Pesheva ◽  
Joerg Nellen ◽  
Hans-Juergen Biersack ◽  
Ranier Probstmeier
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Differentially Expressed ◽  
Cell Phenotype ◽  
Galectin 3 ◽  
Nerve Development

scholarly journals Tissue culture observations relevant to the study of axon-Schwann cell interactions during peripheral nerve development and repair

1987 ◽  
Vol 132 (1) ◽  
pp. 21-34 ◽  
Author(s):  
R. P. Bunge
Keyword(s):  
Tissue Culture ◽  
Schwann Cell ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Basal Lamina ◽  
Heparan Sulphate ◽  
Cell Contact ◽  
Myelinated Nerve ◽  
Nerve Development

During peripheral nerve development the Schwann cell population is expanded so that adequate numbers are available for ensheathment of both nonmyelinated and myelinated nerve fibres. As ensheathment of these fibres progresses each axon--Schwann cell unit becomes surrounded by a basal lamina, providing a unique microtubular framework within the peripheral nerve trunk. Tissue culture studies of pure populations of neurones and Schwann cells cultured separately and in combination indicate that a surface component on the axon provides a mitogenic signal to Schwann cells requiring cell-cell contact. Biochemical, electron microscopic and immunocytochemical analyses of these cultures indicate that Schwann cells in contact with axons are able to generate a basal lamina (containing type IV collagen, laminin and heparan sulphate proteoglycan) and fibrous collagen, without the aid of other cells, and that axonal contact is required for deposition of the basal lamina. The role of Schwann cells and the extracellular matrix they synthesize and organize, as well as the role of the other known products of the Schwann cells in the process of peripheral nerve regeneration, are discussed. It is suggested that the large numbers and advantageous position of the Schwann cells, as well as their ability to provide their own surfaces, a basal lamina and multiple secretory products, may account for their extraordinary ability to foster nerve fibre regeneration.

scholarly journals Insights Into the Role and Potential of Schwann Cells for Peripheral Nerve Repair From Studies of Development and Injury

2021 ◽  
Vol 13 ◽  
Author(s):  
Anjali Balakrishnan ◽  
Lauren Belfiore ◽  
Tak-Ho Chu ◽  
Taylor Fleming ◽  
Rajiv Midha ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Schwann Cells ◽  
Molecular Mechanisms ◽  
Nerve Repair ◽  
Motor Deficits ◽  
Repair Capacity ◽  
Peripheral Nerve Repair ◽  
Cell Replacement

Peripheral nerve injuries arising from trauma or disease can lead to sensory and motor deficits and neuropathic pain. Despite the purported ability of the peripheral nerve to self-repair, lifelong disability is common. New molecular and cellular insights have begun to reveal why the peripheral nerve has limited repair capacity. The peripheral nerve is primarily comprised of axons and Schwann cells, the supporting glial cells that produce myelin to facilitate the rapid conduction of electrical impulses. Schwann cells are required for successful nerve regeneration; they partially “de-differentiate” in response to injury, re-initiating the expression of developmental genes that support nerve repair. However, Schwann cell dysfunction, which occurs in chronic nerve injury, disease, and aging, limits their capacity to support endogenous repair, worsening patient outcomes. Cell replacement-based therapeutic approaches using exogenous Schwann cells could be curative, but not all Schwann cells have a “repair” phenotype, defined as the ability to promote axonal growth, maintain a proliferative phenotype, and remyelinate axons. Two cell replacement strategies are being championed for peripheral nerve repair: prospective isolation of “repair” Schwann cells for autologous cell transplants, which is hampered by supply challenges, and directed differentiation of pluripotent stem cells or lineage conversion of accessible somatic cells to induced Schwann cells, with the potential of “unlimited” supply. All approaches require a solid understanding of the molecular mechanisms guiding Schwann cell development and the repair phenotype, which we review herein. Together these studies provide essential context for current efforts to design glial cell-based therapies for peripheral nerve regeneration.

scholarly journals Schwann Cell-Like Cells Derived from Human Amniotic Mesenchymal Stem Cells Promote Peripheral Nerve Regeneration through a MicroRNA-214/c-Jun Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Wei Chen ◽  
Shune Xiao ◽  
Zairong Wei ◽  
Chengliang Deng ◽  
Kaiyu Nie ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Sciatic Nerve ◽  
Schwann Cell ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Molecular Mechanisms ◽  
Peripheral Nerve Regeneration ◽  
Sciatic Nerve Injury ◽  
Amniotic Mesenchymal Stem Cells

Background. The use of Schwann cell-like cells (SCLCs) derived from stem cells has been introduced as an effective strategy for promoting peripheral nerve regeneration (PNR). However, molecular mechanisms underlying therapeutic transplantation of SCLCs for PNR are often ignored. Objectives. To explore the potential of SCLCs for the treatment of sciatic never injury and investigate the underlying molecule mechanisms. Method. SCLCs differentiated from human amniotic mesenchymal stem cells (hAMSCs) and specific markers of Schwann cells were detected. SCLCs were transplanted into the injured sites of a rat model of sciatic nerve injury, and sciatic nerve functional index (SFI) was determined. Results. SCLCs expressed specific markers of Schwann cells as well as secreted neurotrophic factors. The transplantation of SCLCs into injured sites of a rat model of sciatic nerve injury promoted the functional recovery. With regard to the underlying molecular mechanisms, we identified c-Jun as a negative regulator of the myelination of SCLCs. Moreover, we discovered a novel signaling transduction pathway in SCLCs; that is, miR-214 directly targets c-Jun to promote the myelination of SCLCs. Finally, we demonstrated that miR-214 upon overexpression in SCLCs enhanced the therapeutic effects of SCLCs on sciatic nerve injury. Conclusions. We demonstrate that SCLCs have beneficial effect for myelination. Moreover, our results provide a previously unknown molecular basis underlying the treatment of peripheral nerve injury with SCLCs and also offer a practical strategy for future therapeutic promotion of PNR.

Increasing Calcium Level Limits Schwann Cell Numbers In Vitro following Peripheral Nerve Injury

2017 ◽  
Vol 33 (06) ◽  
pp. 435-440 ◽  
Author(s):  
Kai Yang ◽  
Yuhui Yan ◽  
Lin-Ling Zhang ◽  
Michael Agresti ◽  
Hani Matloub ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Cell Survival ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Normal Control ◽  
Peripheral Nerve Injury ◽  
Calcium Concentration ◽  
Growth Media ◽  
High Calcium

Background After peripheral nerve injury, there is an increase in calcium concentration in the injured nerves. Our previous publications have shown that increase in calcium concentration correlated well with degree of nerve injury and that local infusion of calcitonin has a beneficial effect on nerve recovery. Schwann cells play a pivotal role in regeneration and recovery. We aim to examine cultured Schwann cell survivals in various concentrations of calcium-containing growth media and the effect of calcitonin in such media. Methods To establish baseline in postinjury state, crush injury was induced in male Sprague-Dawley rats' sciatic nerves. Extra- and intraneural calcium concentrations were measured. To study Schwann cell survival, uninjured sciatic nerve segment was harvested and cultured in media containing various amounts of calcium. To study the effect of calcitonin, nerve harvest and culture were done in four additional media: (1) normal control, (2) normal control with calcitonin, (3) high calcium medium, and (4) high calcium medium with calcitonin. Schwann cells were studied and analyzed under fluorescent conditions. Results With increasing calcium concentration, there was a significant decrease in the number of Schwann cells. For the experimental groups, in which calcitonin had been added to the growth medium, there were similar amounts of Schwann cells present in both high and low calcium-containing medium. Conclusion Schwann cells are sensitive to increasing calcium concentration. Calcitonin counteracts the detrimental effects of high calcium on Schwann cell survival. This can have significant future clinical implications for patients with peripheral nerve injuries.

A co-culture microtunnel technique demonstrating a significant contribution of unmyelinated Schwann cells to the acceleration of axonal conduction in Schwann cell-regulated peripheral nerve development

2017 ◽  
Vol 9 (8) ◽  
pp. 678-686 ◽  
Author(s):  
Koji Sakai ◽  
Kenta Shimba ◽  
Kiyoshi Kotani ◽  
Yasuhiko Jimbo
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Conduction Velocity ◽  
Significant Contribution ◽  
Culture Technique ◽  
Axonal Conduction ◽  
Nerve Development

The authors developed a co-culture technique inside a microtunnel and demonstrated that Schwann cells increase axonal conduction velocity before myelination.

scholarly journals Lessons from Injury: How Nerve Injury Studies Reveal Basic Biological Mechanisms and Therapeutic Opportunities for Peripheral Nerve Diseases

2021 ◽  
Author(s):  
Peter Arthur-Farraj ◽  
Michael P. Coleman
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Peripheral Nerves ◽  
Molecular Mechanisms ◽  
Axon Degeneration ◽  
Axon Loss ◽  
Factor C ◽  
Inherited Neuropathies

AbstractSince Waller and Cajal in the nineteenth and early twentieth centuries, laboratory traumatic peripheral nerve injury studies have provided great insight into cellular and molecular mechanisms governing axon degeneration and the responses of Schwann cells, the major glial cell type of peripheral nerves. It is now evident that pathways underlying injury-induced axon degeneration and the Schwann cell injury-specific state, the repair Schwann cell, are relevant to many inherited and acquired disorders of peripheral nerves. This review provides a timely update on the molecular understanding of axon degeneration and formation of the repair Schwann cell. We discuss how nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) and sterile alpha TIR motif containing protein 1 (SARM1) are required for axon survival and degeneration, respectively, how transcription factor c-JUN is essential for the Schwann cell response to nerve injury and what each tells us about disease mechanisms and potential therapies. Human genetic association with NMNAT2 and SARM1 strongly suggests aberrant activation of programmed axon death in polyneuropathies and motor neuron disorders, respectively, and animal studies suggest wider involvement including in chemotherapy-induced and diabetic neuropathies. In repair Schwann cells, cJUN is aberrantly expressed in a wide variety of human acquired and inherited neuropathies. Animal models suggest it limits axon loss in both genetic and traumatic neuropathies, whereas in contrast, Schwann cell secreted Neuregulin-1 type 1 drives onion bulb pathology in CMT1A. Finally, we discuss opportunities for drug-based and gene therapies to prevent axon loss or manipulate the repair Schwann cell state to treat acquired and inherited neuropathies and neuronopathies.

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