Neuronal Neuregulin 1 type III directs Schwann cell migration

Perlin, Julie R.; Lush, Mark E.; Stephens, W. Zac; Piotrowski, Tatjana; Talbot, William S.

doi:10.1242/dev.068072

Cited by 85 publications

(130 citation statements)

References 59 publications

Supporting

Mentioning

122

Contrasting

Order By: Relevance

“…they associate with axons of peripheral nerves. Schwann cells depend on Nrg1/ErbB signaling for migration along the axon tracts and for proliferation, and are basically absent in mice or zebrafish that lack Nrg1, ErbB2 or ErbB3 (Meyer and Birchmeier, 1995;Riethmacher et al, 1997;Woldeyesus et al, 1999;Lyons et al, 2005;Perlin et al, 2011). The Nrg1 signal that drives Schwann cell development is provided by neurons, and presented in the axolemma.…”

Section: Schwann Cell Precursorsmentioning

confidence: 99%

“…Interestingly, different isoforms take over distinct functions in vivo. For instance type III and type I Nrg1 are produced by all or just a subset of sensory neurons, respectively, and have distinct functions in myelination and muscle spindle induction (Meyer and Birchmeier, 1995;Hippenmeyer et al, 2002;Perlin et al, 2011;Cheret et al, 2013). Nrg1 isoforms are produced as soluble membrane-bound proteins.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuregulin/ErbB Signaling in Developmental Myelin Formation and Nerve Repair

Birchmeier

Bennett

2016

Current Topics in Developmental Biology

View full text Add to dashboard Cite

Myelin is essential for rapid and accurate conduction of electrical impulses by axons in the central and peripheral nervous system. Myelin is formed in the early postnatal period, and developmental myelination in the peripheral nervous system (PNS) depends on axonal signals provided by Nrg1/ErbB receptors. In addition, Nrg1 is required for effective nerve repair and remyelination in adulthood. We discuss here similarities and differences in Nrg1/ErbB functions in developmental myelination and remyelination after nerve injury.

show abstract

Section: Schwann Cell Precursorsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuregulin/ErbB Signaling in Developmental Myelin Formation and Nerve Repair

Birchmeier

Bennett

2016

Current Topics in Developmental Biology

View full text Add to dashboard Cite

show abstract

“…Transgenic fish harboring the UAS:hNrg1typeIII transgene were described previously (Perlin et al, 2011). S1101:Gal4 transgenic fish express the Gal4 transcriptional activator in all neurons (Scott et al, 2007).…”

Section: Zebrafish Strainsmentioning

confidence: 99%

“…To determine whether activation of the Nrg1 signaling pathway is sufficient to rescue peripheral myelination in gpr126 mutants, we analyzed fish containing a human NRG1 type III transgene under control of the UAS promoter sequence (Perlin et al, 2011) in a gpr126 st49/st49 background. A previous study shows that this transgene causes ectopic Schwann cell migration as well as an expansion of mbp expression in zebrafish (Perlin et al, 2011).…”

Section: Overexpression Of Nrg1 Type III Does Not Rescue Myelination mentioning

confidence: 99%

Analysis of Gpr126 function defines distinct mechanisms controlling the initiation and maturation of myelin

Glenn

Talbot

2013

Development

Self Cite

View full text Add to dashboard Cite

SUMMARYIn peripheral nerves, Schwann cells form the myelin sheath, which allows the efficient propagation of action potentials along axons. The transcription factor Krox20 regulates the initiation of myelination in Schwann cells and is also required to maintain mature myelin. The adhesion G protein-coupled receptor (GPCR) Gpr126 is essential for Schwann cells to initiate myelination, but previous studies have not addressed the role of Gpr126 signaling in myelin maturation and maintenance. Through analysis of Gpr126 in zebrafish, we define two distinct mechanisms controlling the initiation and maturation of myelin. We show that gpr126 mutant Schwann cells elaborate mature myelin sheaths and maintain krox20 expression for months, provided that the early signaling defect is bypassed by transient elevation of cAMP. At the onset of myelination, Gpr126 and protein kinase A (PKA) function as a switch that allows Schwann cells to initiate krox20 expression and myelination. After myelination is initiated, krox20 expression is maintained and myelin maturation proceeds independently of Gpr126 signaling. Transgenic analysis indicates that the Krox20 cis-regulatory myelinating Schwann cell element (MSE) becomes active at the onset of myelination and that this activity is dependent on Gpr126 signaling. Activity of the MSE declines after initiation, suggesting that other elements are responsible for maintaining krox20 expression in mature nerves. We also show that elevated cAMP does not initiate myelination in the absence of functional Neuregulin 1 (Nrg1) signaling. These results indicate that the mechanisms regulating the initiation of myelination are distinct from those mediating the maturation and maintenance of myelin.

show abstract

“…As mentioned before, there has a close relationship between NRG1 and SCs. NRG1 secreted by peripheral axons has previously been identified as an essential factor for SCs proliferation and migration 24 . SCs play a critical role in promoting neuronal regeneration and differentiation in the peripheral nervous system by expressing neurotrophic factors, including NGF.…”

Section: Exogenous Nrg1 Can Inhibit Diabetic Neuropathic Painmentioning

confidence: 99%

Exogenous neuregulin-1 attenuates STZ-induced diabetic peripheral neuropathic pain in rats

Zhou¹,

Xia²,

Liu³

et al. 2017

Acta Cir. Bras.

View full text Add to dashboard Cite

Purpose: To investigate whether modulating NRG1 could attenuate diabetic neuropathic pain and analyze the underlying mechanism. Methods: Male SD rats were randomly divided into control group, diabetic group, NRG1 intervention group. After STZ-induced 2 weeks, NRG1 intervention daily for consecutive 7 days. 4 weeks after NRG1 intervention, both the mechanical withdrawal threshold and the morphological changes of the dorsal root ganglion and sural nerve were observed. Meanwhile, the expression of NGF, IL-1β, TNF-α in spinal cord were determined. Results: Compared with the diabetic group, NRG1 treatment improved the mechanical withdrawal threshold in diabetic rats, pathological changes of dorsal root ganglion and sural nerve were alleviated by NRG1 treatment with electron microscopy imagine. Moreover, compared with the control group, the expression of NGF was significantly decreased and the production of IL-1β, TNF-α were markedly induced in diabetic group. Furthermore, NRG1 treatment could normalized the above effect as compared to diabetic group. Conclusion: NRG1 exerted positive effects on the behavioral and pathological changes of rats with STZ-induced diabetic neuropathic pain, the underlying mechanism might be related to the promotion of NGF excretion and the inhibition of inflammatory cytokines excretion.

show abstract

Neuronal Neuregulin 1 type III directs Schwann cell migration

Cited by 85 publications

References 59 publications

Neuregulin/ErbB Signaling in Developmental Myelin Formation and Nerve Repair

Neuregulin/ErbB Signaling in Developmental Myelin Formation and Nerve Repair

Analysis of Gpr126 function defines distinct mechanisms controlling the initiation and maturation of myelin

Exogenous neuregulin-1 attenuates STZ-induced diabetic peripheral neuropathic pain in rats

Contact Info

Product

Resources

About