Schwann cell proliferation during Wallerian degeneration is not necessary for regeneration and remyelination of the peripheral nerves: Axon-dependent removal of newly generated Schwann cells by apoptosis

Yang, David P.; Zhang, Dan P.; Mak, Kimberley S.; Bonder, Daniel E.; Pomeroy, Scott L.; Kim, Haesun A.

doi:10.1016/j.mcn.2008.01.017

Cited by 94 publications

(79 citation statements)

References 49 publications

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“…A previous investigation of crushed sciatic nerves (Yang et al 2008) proves that prevention of Schwann cell proliferation has no adverse effects on regeneration and remyelination under conditions preserving the connectivity of both stumps. However, a contradictory study characterizing different conditions in transected nerves, where the cut ends are separated, show impaired axonal regeneration following blocking of Schwann cell proliferation and migration (Chen et al 2005).…”

Section: Neurotrophic Factorsmentioning

confidence: 91%

Extrinsic cellular and molecular mediators of peripheral axonal regeneration

Bosse

2012

Cell Tissue Res

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The ability of injured peripheral nerves to regenerate and reinnervate their original targets is a characteristic feature of the peripheral nervous system (PNS). On the other hand, neurons of the central nervous system (CNS), including retinal ganglion cell (RGC) axons, are incapable of spontaneous regeneration. In the adult PNS, axonal regeneration after injury depends on well-orchestrated cellular and molecular processes that comprise a highly reproducible series of degenerative reactions distal to the site of injury. During this fine-tuned process, named Wallerian degeneration, a remodeling of the distal nerve fragment prepares a permissive microenvironment that permits successful axonal regrowth originating from the proximal nerve fragment. Therefore, a multitude of adjusted intrinsic and extrinsic factors are important for surviving neurons, Schwann cells, macrophages and fibroblasts as well as endothelial cells in order to achieve successful regeneration. The aim of this review is to summarize relevant extrinsic cellular and molecular determinants of successful axonal regeneration in rodents that contribute to the regenerative microenvironment of the PNS.

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Section: Neurotrophic Factorsmentioning

confidence: 91%

Extrinsic cellular and molecular mediators of peripheral axonal regeneration

Bosse

2012

Cell Tissue Res

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“…Although Schwann cells reenter the cell cycle after injury, and their number in the distal stump increases severalfold, regeneration following a crush injury is equally effective in mice in which Schwann cell proliferation is inhibited (Kim et al 2000;Atanasoski et al 2001; Cite this article as Cold Spring Harb Perspect Biol 2015;7:a020487 on May 10, 2018 -Published by Cold Spring Harbor Laboratory Press http://cshperspectives.cshlp.org/ Downloaded from Yang et al 2008). This suggests that the conversion of myelin Schwann cells to repair Schwann cells does not depend on reentry to the cell cycle.…”

Section: The Schwann Cell Injury Response In the Distal Stumpmentioning

confidence: 99%

Schwann Cells: Development and Role in Nerve Repair

Jessen

Mirsky

Lloyd

2015

Cold Spring Harb Perspect Biol

554

518

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Schwann cells develop from the neural crest in a well-defined sequence of events. This involves the formation of the Schwann cell precursor and immature Schwann cells, followed by the generation of the myelin and nonmyelin (Remak) cells of mature nerves. This review describes the signals that control the embryonic phase of this process and the organogenesis of peripheral nerves. We also discuss the phenotypic plasticity retained by mature Schwann cells, and explain why this unusual feature is central to the striking regenerative potential of the peripheral nervous system (PNS).T he myelin and nonmyelin (Remak) Schwann cells of adult nerves originate from the neural crest in well-defined developmental steps ( Fig. 1). This review focuses on embryonic development (for additional information on myelination, see Salzer 2015). We also discuss how the ability to change between differentiation states, a characteristic attribute of developing cells, is retained by mature Schwann cells, and explain how the ability of Schwann cells to change phenotype in response to injury allows the peripheral nervous system (PNS) to regenerate after damage. TWO TYPES OF EMBRYONIC NERVESAdult nerves are stable structures in which the nerve fibers are protected structurally by a collagen-rich, vascularized extracellular matrix (the endoneurium) linked to the basal lamina surrounding each axon -Schwann cell unit. The endoneurial environment is further protected by a surrounding multilayered cellular tube (the perineurium) that shields the nerve fibers from unwanted cells and molecules (Fig. 2).A more dynamic and radically different structure, reminiscent of axon -glial organization in the central nervous system (CNS), is seen in early embryonic nerves (embryo day E14/15 in rat hind limb and E12/13 in mouse). These nerves consist of tightly packed axons and flattened, glial cell processes without significant extracellular space, matrix, or basal lamina. The glial cell bodies lie among the axons inside the nerve or at the nerve surface. These cells represent the first stage of the Schwann cell lineage, Schwann cell precursors (Figs. 3 and 4).

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“…Scale bar 20 lm. d Compared with the control, the protein level of P0 remained low after treatment with cAMP in SYF2-specific siRNA Schwann cells proliferate and redifferentiate about 5 days following injury, providing a permissive environment for nerve regeneration (Cheng et al 2007;Fawcett and Keynes 1990;Ji et al 2010;Yang et al 2008). As to cell differentiation, Schwann cells stem from neural crest cells, and experience extensive migration, proliferation, and maturation before they terminally differentiate (Jessen and Mirsky 2005).…”

Section: Scale Bars 50 Lmmentioning

confidence: 99%

Involvement of Upregulated SYF2 in Schwann Cell Differentiation and Migration After Sciatic Nerve Crush

et al. 2014

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SYF2 is a putative homolog of human p29 in Saccharomyces cerevisiae. It seems to be involved in pre-mRNA splicing and cell cycle progression. Disruption of SYF2 leads to reduced α-tubulin expression and delayed nerve system development in zebrafish. Due to the potential of SYF2 in modulating microtubule dynamics in nervous system, we investigated the spatiotemporal expression of SYF2 in a rat sciatic nerve crush (SNC) model. We found that SNC resulted in a significant upregulation of SYF2 from 3 days to 1 week and subsequently returned to the normal level at 4 weeks. At its peak expression, SYF2 distributed predominantly in Schwann cells. In addition, upregulation of SYF2 was approximately in parallel with Oct-6, and numerous Schwann cells expressing SYF2 were Oct-6 positive. In vitro, we observed enhanced expression of SYF2 during the process of cyclic adenosine monophosphate (cAMP)-induced Schwann cell differentiation. SYF2-specific siRNA-transfected Schwann cells did not show significant morphological change in the process of Schwann cell differentiation. Also, we found shorter and disorganized microtubule structure and a decreased migration in SYF2-specific siRNA-transfected Schwann cells. Together, these findings indicated that the upregulation of SYF2 was associated with Schwann cell differentiation and migration following sciatic nerve crush.

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Schwann cell proliferation during Wallerian degeneration is not necessary for regeneration and remyelination of the peripheral nerves: Axon-dependent removal of newly generated Schwann cells by apoptosis

Cited by 94 publications

References 49 publications

Extrinsic cellular and molecular mediators of peripheral axonal regeneration

Extrinsic cellular and molecular mediators of peripheral axonal regeneration

Schwann Cells: Development and Role in Nerve Repair

Involvement of Upregulated SYF2 in Schwann Cell Differentiation and Migration After Sciatic Nerve Crush

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