Chronically denervated rat schwann cells respond to GGF in vitro

Li, H.; Wigley, Caroline B.; Hall, Susan

doi:10.1002/(sici)1098-1136(199811)24:3<290::aid-glia3>3.0.co;2-6

Cited by 56 publications

(25 citation statements)

References 57 publications

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“…In agreement with this, treatment of chronically denervated nerve explants with recombinant NRG1 type II in the presence of forskolin increased the number of SCs migrating from the explants [97]. Furthermore, cultured peritoneal macrophages express erbB2, erbB3 and, erbB4 and in response to recombinant NRG1 β-EGF domain, show enhanced motility ( Figure 4) [98].…”

Section: Potential Mechanisms Of Action Of Nrg1 Signaling In Periphersupporting

confidence: 70%

“…Treatment of SC neuronal co-cultures with recombinant NRG1 type II has been shown to dose-dependently stimulate proliferation of SCs [96,97]. The use of a pharmacological inhibitor of all erbB receptors produced a reduction in SC proliferation 2 days after sciatic nerve axotomy [80].…”

Section: Potential Mechanisms Of Action Of Nrg1 Signaling In Periphermentioning

confidence: 99%

“…Given the critical role of these cells for axon regeneration, this is likely to significantly impair functional recovery. There is evidence that chronically denervated SCs can still respond to NRG1 in vitro [97]. If NRG1 could provide a means to maintain SCs in a healthy state until they re-establish a relationship with axons, this could provide a means to promote functional recovery, particularly after proximal lesions such as brachial plexus injuries.…”

Section: Potential Mechanisms Of Action Of Nrg1 Signaling In Periphermentioning

confidence: 99%

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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: Potential Mechanisms Of Action Of Nrg1 Signaling In Periphersupporting

confidence: 70%

Section: Potential Mechanisms Of Action Of Nrg1 Signaling In Periphermentioning

confidence: 99%

Section: Potential Mechanisms Of Action Of Nrg1 Signaling In Periphermentioning

confidence: 99%

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

Fricker

Bennett

2011

Future Neurol.

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“…This includes non-neoplastic Schwann cells; earlier studies of NRG-1β effects on the migration of these glia did not utilize laminin as a substrate or compare their relative rates of migration on different substrates (Meintanis et al, 2001; Li et al, 1998; Mahanthappa et al, 1996). It is therefore currently unclear whether the tendency of NRG-1β to promote migration preferentially on laminin is peculiar to MPNST cells.…”

Section: Discussionmentioning

confidence: 99%

Neuregulin‐1β and neuregulin‐1α differentially affect the migration and invasion of malignant peripheral nerve sheath tumor cells

Eckert

Byer

Clodfelder‐Miller

et al. 2009

Glia

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Malignant peripheral nerve sheath tumors (MPNSTs) are the most common malignancy associated with neurofibromatosis type 1 (NF1). These Schwann cell lineage-derived sarcomas aggressively invade adjacent nerve and soft tissue, frequently precluding surgical resection. Little is known regarding the mechanisms underlying this invasive behavior. We have shown that MPNSTs express neuregulin-1 (NRG-1) β isoforms, which promote Schwann cell migration during development, and NRG-1α isoforms, whose effects on Schwann cells are poorly understood. Hypothesizing that NRG-1β and/or NRG-1α promote MPNST invasion, we found that NRG-1β promoted MPNST migration in a substrate-specific manner, markedly enhancing migration on laminin but not on collagen type I or fibronectin. The NRG-1 receptors erbB3 and erbB4 were present in MPNST invadopodia (processes mediating invasion), partially colocalized with focal adhesion kinase and the laminin receptor β1-integrin and coimmunoprecipitated with β1-integrin. NRG-1β stimulated human and murine MPNST cell migration and invasion in a concentration-dependent manner in three-dimensional migration assays, acting as a chemotactic factor. Both baseline and NRG-1β induced migration were erbB-dependent and required the action of MEK 1/2, SAPK/JNK, PI-3 kinase, Src family kinases and ROCK-I/II. In contrast, NRG-1α had no effect on the migration and invasion of some MPNST lines and inhibited the migration of others. While NRG-1β potently and persistently activated Erk 1/2, SAPK/JNK, Akt and Src family kinases, NRG-1α did not activate Akt and activated these other kinases with kinetics distinct from those evident in NRG-1β stimulated cells. These findings suggest that NRG-1β enhances MPNST migration and that NRG-1β and NRG-1α differentially modulate this process.

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“…Furthermore, Schwann cell ability to respond to signals of axonal degeneration following peripheral nerve injury is significantly reduced after 2 months 10. These neurobiological aspects indicate that (partial) nerve transection should be determined early and repaired at least within 3 months, before irreversible loss occurs.…”

Section: Discussionmentioning

confidence: 99%

Unusual radial nerve injury by a locking compression plate for humerus fracture

Kinaci¹,

Kloen²,

Videler³

et al. 2014

BMJ Case Reports

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The management of primary and secondary radial nerve palsy associated with humeral shaft fractures is still controversial. Radial nerve function is likely to return spontaneously after primary as well as secondary radial nerve palsy in the absence of any level of neurotmesis. Identification and protection of the radial nerve during surgery may prevent secondary nerve palsy, but is not always performed and depends on the location of the fracture, and the experience and preference of the surgeon. We report a case of a healthy 40-year-old woman, referred to our hospital with a complete radial nerve palsy and a failed plate fixation of a right humeral shaft fracture. During exploration of the radial nerve and surgical revision of the fracture, we found the nerve entrapped by the plate and partially transected by a screw. Full recovery of radial nerve function occurred after neurolysis and microscopic neurorrhaphy.

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Chronically denervated rat schwann cells respond to GGF in vitro

Cited by 56 publications

References 57 publications

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

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

Neuregulin‐1β and neuregulin‐1α differentially affect the migration and invasion of malignant peripheral nerve sheath tumor cells

Unusual radial nerve injury by a locking compression plate for humerus fracture

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