Myelin synthesis in the peripheral nervous system

Garbay, Bertrand; Heape, Anthony M.; Sargueil, Françoise; Cassagne, Claude

doi:10.1016/s0301-0082(99)00049-0

Cited by 272 publications

(266 citation statements)

References 392 publications

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“…It has long been observed that in addition to the requirement of axons for the maintenance of a myelinating SC phenotype, the axon diameter determines whether an axon is myelinated and the thickness of the myelin sheath [48][49][50]. NRG1 is now known to be a key axonderived factor in determining axon ensheathment and peripheral myelin thickness.…”

Section: Myelinationmentioning

confidence: 99%

The Role of Neuregulin-1 In the Response To Nerve Injury

Fricker

Bennett

2011

Future Neurol.

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Axons and Schwann cells exist in a highly interdependent relationship: damage to one cell type invariably leads to pathophysiological changes in the other. Greater understanding of communication between these cell types will not only give insight into peripheral nerve development, but also the reaction to and recovery from peripheral nerve injury. The type III isoform of neuregulin-1 (NRG1) has emerged as a key signaling factor that is expressed on axons and, through binding to erbB2/3 receptors on Schwann cells, regulates multiple phases of their development. In adulthood, NRG1 is dispensable for the maintenance of the myelin sheath; however, this factor is required for both axon regeneration and remyelination following nerve injury. The outcome of NRG1 signaling depends on interactions with other pathways within Schwann cells such as Notch, integrin and cAMP signaling. In certain circumstances, this signaling pathway may be maladaptive; for instance, direct binding of Mycobacterium leprae onto erbB2 receptors produces excessive activation and can actually promote demyelination. Attempts to modulate this pathway in order to promote nerve repair will therefore need to give consideration to the exact isoform used, as well as how it is processed and the context in which it is presented to the Schwann cell. Keywordsneuregulin-1; neuropathy; peripheral nerve injury; regeneration; remyelination; repair; Schwann cell Peripheral nerve injury causes significant morbidity and reduced quality of life as a consequence of weakness, sensory loss and neuropathic pain. In total, 6% of the elderly population suffer from peripheral neuropathy [1], which can be caused by metabolic diseases such as diabetes, inherited genetic disorders such as Charcot-Marie-Tooth disease, infectious and inflammatory disorders including Guillan-Barré syndrome and traumatic injury to the nerve (which alone effects up to 300,000 people in Europe per year [1,2]). In contrast to the CNS, peripheral nerves have a significant regenerative capacity [3]; however, in patients, regeneration and the clinical outcome are often poor. Axons regenerate at a rate of approximately 1 mm per day, depending on the site of the lesion. There may be a delay of months if not years before the target zone is re-innervated, and by this time, the target organ and supporting cells may have irreversibly changed, becoming much less receptive to reinnervation. The current approaches to peripheral nerve repair following nerve transection are either to surgically suture the nerve or to bridge the gap between the two cut ends. Financial & competing interests disclosureThe authors have no other rel evant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript. Europe PMC Funders Group NRGs & the PNSNRGs Neuregulins are a family of growth factors en...

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Section: Myelinationmentioning

confidence: 99%

The Role of Neuregulin-1 In the Response To Nerve Injury

Fricker

Bennett

2011

Future Neurol.

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“…Myelin synthesis by Schwann cells is an important process in the regeneration of injured peripheral nerves as well as in the normal development of the peripheral nervous system (PNS) [4,9,12]. It is well known that myelination by Schwann is regulated by various endogenous modulators including extracellular matrix proteins, neurotrophic factors, and cytokines [3,4].…”

Section: Interleukin-6 Upregulates the Expression Of Pmp22 In Culturementioning

confidence: 99%

“…PMP22 is a tetraspan glycoprotein vigorously produced by myelinating Schwann cells [9,18,24,25]. Despite its abundant presence in the compact myelin, the physiological role of PMP22 has not been fully clarified.…”

Section: Interleukin-6 Upregulates the Expression Of Pmp22 In Culturementioning

confidence: 99%

“…expression in sciatic nerve is strongly upregulated during the postnatal period [9,18,24,25] and during nerve regeneration after injury [9,24,25]. Duplication of the PMP22 genes is associated with hereditary demyelinating neuropathies, such as Charcot-Marie-Tooth disease type 1A , and deletion of a single gene copy leads to hereditary neuropathy with liability to pressure palsies [25].…”

Section: Interleukin-6 Upregulates the Expression Of Pmp22 In Culturementioning

confidence: 99%

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Interleukin-6 upregulates the expression of PMP22 in cultured rat Schwann cells via a JAK2-dependent pathway

Ito

Ikeda

Tomita

et al. 2010

Neuroscience Letters

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The interleukin-6 (IL-6) family of cytokines is thought to be involved in the development and regeneration of peripheral nerves; however, their roles in myelination remain unclear. In this study, we examined the effects of IL-6 on the expression of genes for compact myelin proteins using Schwann cell cultures prepared by multiple explantation of adult rat sciatic nerves. In semi-quantitative reverse transcription-polymerase chain reaction analysis, stimulation of Schwann cells with IL-6 significantly increased the mRNA level of peripheral myelin protein 22 (PMP22), but not those of myelin protein zero and myelin basic protein. The increase in PMP22 mRNA was markedly suppressed by AG490, a Janus kinase 2 (JAK2) inhibitor, but not significantly by PD098059, a mitogen-activated protein kinase kinase inhibitor. Immunocytochemical staining revealed that IL-6 enhanced immunoreactivities for the phosphorylated forms of both JAK2 and signal transducer and activator of transcription 3 (STAT3), as well as that for PMP22. These results indicate that IL-6 can enhance PMP22 production in Schwann cells via a JAK2-dependent pathway by probably activating STAT3 and thus may contribute to myelination. E-mail address: shigeruy@med.kanazawa-u.ac.jp (S. Yokoyama). *Manuscript Click here to view linked References 2 ABSTRACTThe interleukin-6 (IL-6) family of cytokines is thought to be involved in the development

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“…Peripheral myelin gene expression [Myelin Protein Zero (MPZ) and Peripheral Myelin Protein 22 (PMP22)] is tightly regulated (1). Myelin gene expression is stimulated during the myelination process, which occurs in rodents between postnatal days 1 and 21 (2). Afterward, those genes are expressed at lower levels, sufficient to maintain myelin turnover.…”

mentioning

confidence: 99%

Lithium enhances remyelination of peripheral nerves

Makoukji

Belle

Meffre

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

104

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Glycogen synthase kinase 3β (GSK3β) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or anti-inflammatory agents. We studied the influence of LiCl on the remyelination of peripheral nerves. We showed that the treatment of adult mice with LiCl after facial nerve crush injury stimulated the expression of myelin genes, restored the myelin structure, and accelerated the recovery of whisker movements. LiCl treatment also promoted remyelination of the sciatic nerve after crush. We also demonstrated that peripheral myelin gene MPZ and PMP22 promoter activities, transcripts, and protein levels are stimulated by GSK3β inhibitors (LiCl and SB216763) in Schwann cells as well as in sciatic and facial nerves. LiCl exerts its action in Schwann cells by increasing the amount of β-catenin and provoking its nuclear localization. We showed by ChIP experiments that LiCl treatment drives β-catenin to bind to T-cell factor/lymphoid-enhancer factor response elements identified in myelin genes. Taken together, our findings open perspectives in the treatment of nerve demyelination by administering GSK3β inhibitors such as lithium.Wnt/β-catenin | neuropathy

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Myelin synthesis in the peripheral nervous system

Cited by 272 publications

References 392 publications

The Role of Neuregulin-1 In the Response To Nerve Injury

The Role of Neuregulin-1 In the Response To Nerve Injury

Interleukin-6 upregulates the expression of PMP22 in cultured rat Schwann cells via a JAK2-dependent pathway

Lithium enhances remyelination of peripheral nerves

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