Linkage Between Axonal Ensheathment and Basal Lamina Production by Schwann Cells

Bunge, R P; Bunge, M. B.; Eldridge, Charles F.

doi:10.1146/annurev.ne.09.030186.001513

Cited by 278 publications

(128 citation statements)

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“…The axon signals for regulating Schwann cell differentiation are known to include both proteins encoded by the neuregulin gene (NRG) signaling through the erbB family of receptors, adhesion molecules such as L1 and N-cadherin and neurotrophic factors such as brainderived neurotrophic factor (BDNF) (34)(35)(36)(37). It has been suggested that cell adhesion molecules on the axon surface as well as signals from the extracellular matrix and neurotrophins are also required for myelination to proceed efficiently and accurately.…”

Section: Discussionmentioning

confidence: 99%

Deletion of the mouse RegIIIβ (Reg2) gene disrupts ciliary neurotrophic factor signaling and delays myelination of mouse cranial motor neurons

Tebar

Géranton

Parsons-Perez

et al. 2008

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

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A large number of cytokines and growth factors support the development and subsequent maintenance of postnatal motor neurons. RegIII␤, also known as Reg2 in rat and HIP/PAP1 in humans, is a member of a family of growth factors found in many areas of the body and previously shown to play an important role in both the development and regeneration of subsets of motor neurons. It has been suggested that RegIII␤ expressed by motor neurons is both an obligatory intermediate in the downstream signaling of the leukemia inhibitory factor/ciliary neurotrophic factor (CNTF) family of cytokines, maintaining the integrity of motor neurons during development, as well as a powerful influence on Schwann cell growth during regeneration of the peripheral nerve. Here we report that in mice with a deletion of the RegIII␤ gene, motor neuron survival was unaffected up to 28 weeks after birth. However, there was no CNTF-mediated rescue of neonatal facial motor neurons after axotomy in KO animals when compared with wild-type. In mice, RegIII␤ positive motor neurons are concentrated in cranial motor nuclei that are involved in the patterning of swallowing and suckling. We found that suckling was impaired in RegIII␤ KO mice and correlated this with a significant delay in myelination of the hypoglossal nerve. In summary, we propose that RegIII␤ has an important role to play in the developmental fine-tuning of neonatal motor behaviors mediating the response to peripherally derived cytokines and growth factors and regulating the myelination of motor axons.Schwann cells ͉ suckling ͉ hypoglossal nerve ͉ LIF

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Section: Discussionmentioning

confidence: 99%

Deletion of the mouse RegIIIβ (Reg2) gene disrupts ciliary neurotrophic factor signaling and delays myelination of mouse cranial motor neurons

Tebar

Géranton

Parsons-Perez

et al. 2008

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

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“…For example, the ECM molecules of the basal lamina are crucial for both axonal elongation and remyelination (Bunge et al, 1986;Reichardt and Tomaselli, 1991). Schwann cells react to changes in the composition of the ECM after nerve lesion.…”

Section: Discussionmentioning

confidence: 99%

Mice Lacking Protease Nexin-1 Show Delayed Structural and Functional Recovery after Sciatic Nerve Crush

Lino¹,

Atanasoski²,

Kvajo³

et al. 2007

J. Neurosci.

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Multiple molecular mechanisms influence nerve regeneration. Because serine proteases were shown to affect peripheral nerve regeneration, we performed nerve crush experiments to study synapse reinnervation in adult mice lacking the serpin protease nexin-1 (PN-1). PN-1 is a potent endogenous inhibitor of thrombin, trypsin, tissue plasminogen activators (tPAs), and urokinase plasminogen activators. Compared with the wild type, a significant delay in synapse reinnervation was detected in PN-1 knock-out (KO) animals, which was associated with both reduced proliferation and increased apoptosis of Schwann cells. Various factors known to affect Schwann cells were also altered. Fibrin deposits, tPA activity, mature BDNF, and the low-affinity p75 neurotrophin receptor were increased in injured sciatic nerves of mutant mice. To test whether the absence of PN-1 in Schwann cells or in the axon caused delay in reinnervation, PN-1 was overexpressed exclusively in the nerves of PN-1 KO mice. Neuronal PN-1 expression did not rescue the delayed reinnervation. The results suggest that Schwann cell-derived PN-1 is crucial for proper reinnervation through its contribution to the autocrine control of proliferation and survival. Thus, the precise balance between distinct proteases and serpins such as PN-1 can modulate the overall impact on the kinetics of recovery.

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“…The importance of Schwann cell interaction with ECM as a prerequisite for myelination is well established (Bunge et al, 1986). Several matrix protein-receptor interactions that are important for Schwann cell myelination have been described.…”

Section: Discussionmentioning

confidence: 99%

Glypican-1 and α4(V) Collagen Are Required for Schwann Cell Myelination

Chernousov

Rothblum²,

Stahl³

et al. 2006

J. Neurosci.

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Linkage Between Axonal Ensheathment and Basal Lamina Production by Schwann Cells

Cited by 278 publications

References 0 publications

Deletion of the mouse RegIIIβ (Reg2) gene disrupts ciliary neurotrophic factor signaling and delays myelination of mouse cranial motor neurons

Deletion of the mouse RegIIIβ (Reg2) gene disrupts ciliary neurotrophic factor signaling and delays myelination of mouse cranial motor neurons

Mice Lacking Protease Nexin-1 Show Delayed Structural and Functional Recovery after Sciatic Nerve Crush

Glypican-1 and α4(V) Collagen Are Required for Schwann Cell Myelination

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