Schwann Cells in Central Regeneration<sup>a</sup>

Bunge, Richard P.

doi:10.1111/j.1749-6632.1991.tb15614.x

Cited by 15 publications

(7 citation statements)

References 16 publications

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“…Schwann cells have been shown to facilitate axonal regeneration, a process that depends on secreted neurotrophic factors, extracellular matrix and cell adhesion molecules [21][22][23], and previous studies showed that BMSCs can be transdifferentiated in vitro in presence of Brain-Derived Neurotrophic Factor (BDNF) or Nervous Growth Factor (NGF) [24]. Keeping in mind that adult Schwann cells and astroglial cells can release these neurotrophic factors [25], it is possible to accept that neuronal transdifferentiation of BMSCs can be obtained in vivo when they are grafted into nervous tissue, because of the presence of environmental neurotrophic factors.…”

Section: Discussionmentioning

confidence: 99%

Neurotrophic Schwann-cell factors induce neural differentiation of bone marrow stromal cells

Zurita

Vaquero²,

Oya³

et al. 2007

NeuroReport

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Neural transdifferentiation of bone marrow stromal cells has been questioned, because cell fusion could explain the development of new cell types, misinterpreted as transdifferentiated cells. We performed here cocultures of bone marrow stromal cells and Schwann cells, without possibility that both cell types can establish contact. In these conditions, bone marrow stromal cells expressed nestin 4 h after beginning cocultures, and strong expression of neuronal markers was disclosed at 72 h, increasing at 1 and 2 weeks. Our results support that neural transdifferentiation of bone marrow stromal cells is induced by soluble factors provided by glial cells, and suggest that cell fusion should not be significant when local bone marrow stromal cells administration for neural repair is considered.

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Section: Discussionmentioning

confidence: 99%

Neurotrophic Schwann-cell factors induce neural differentiation of bone marrow stromal cells

Zurita

Vaquero²,

Oya³

et al. 2007

NeuroReport

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“…126 Another potential benefit of these cells is the ability to harvest them from an autologous source, such as the sural nerve. The work of Bunge 18 at the Miami Project has explored this possibility since the early 1990s. A limitation of this technique, however, appears to be that regenerating CNS axons readily grow into the permissive environment that these cells provide; however, they are not prone to growing out of them and back into the hostile CNS environment.…”

Section: Schwann Cellsmentioning

confidence: 99%

Protection and repair of the injured spinal cord: a review of completed, ongoing, and planned clinical trials for acute spinal cord injury

Hawryluk

Rowland

Kwon

et al. 2008

FOC

208

114

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Over the past 2 decades, advances in understanding the pathophysiology of spinal cord injury (SCI) have stimulated the recent emergence of several therapeutic strategies that are being examined in Phase I/II clinical trials. Ten randomized controlled trials examining methylprednisolone sodium succinate, tirilizad mesylate, monosialotetrahexosylganglioside, thyrotropin releasing hormone, gacyclidine, naloxone, and nimodipine have been completed. Although the primary outcomes in these trials were laregely negative, a secondary analysis of the North American Spinal Cord Injury Study II demonstrated that when administered within 8 hours of injury, methylprednisolone sodium succinate was associated with modest clinical benefits, which need to be weighed against potential complications. Thyrotropin releasing hormone (Phase II trial) and monosialotetrahexosylganglioside (Phase II and III trials) also showed some promise, but we are unaware of plans for future trials with these agents. These studies have, however, yielded many insights into the conduct of clinical trials for SCI. Several current or planned clinical trials are exploring interventions such as early surgical decompression (Surgical Treatment of Acute Spinal Cord Injury Study) and electrical field stimulation, neuroprotective strategies such as riluzole and minocycline, the inactivation of myelin inhibition by blocking Nogo and Rho, and the transplantation of various cellular substrates into the injured cord. Unfortunately, some experimental and poorly characterized SCI therapies are being offered outside a formal investigational structure, which will yield findings of limited scientific value and risk harm to patients with SCI who are understandably desperate for any intervention that might improve their function. Taken together, recent advances suggest that optimism for patients and clinicians alike is justified, as there is real hope that several safe and effective therapies for SCI may become available over the next decade.

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“…As others (Wrathall et al, 1982;Paino and Bunge, 1991;Li and Raisman, 1994;Kromer and Cornbrooks, 1985;Neuberger et al, 1992;Montero-Menei et al, 1992), we have grafted into the lesion a Schwann cell suspension. Indeed, peripheral nerve grafts have been shown to support central neuron regeneration provided they contain living cells including Schwann cells, and, furthermore, purified Schwann cells expanded in culture also promote central neuron regeneration (Li and Raisman, 1994;Kromer and Cornbrooks, 1985;Paino and Bunge, 1991;Bunge, 1991). More specifically, the following issues have been addressed.…”

Section: Introductionmentioning

confidence: 99%

Effects of Schwann cell transplantation in a contusion model of rat spinal cord injury

et al. 1996

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Cultured Schwann cells were transplanted at various delays into a spinal cord contusion injury performed at low thoracic level in adult female rats. The Schwann cells were purified from the dorsal root ganglia of adult syngeneic animals. The transplants were well tolerated, and the transplanted Schwann cells invaded the injured spinal cord. As quantified using video image analysis, the survival and growth of the transplanted cells were poor when the grafting procedure was performed 3–4 days after injury and very good when performed immediately or 10 days after injury, in which cases post‐traumatic micro‐ and macrocavitation were strongly reduced. In animals grafted immediately after injury but not in animals grafted after 10 days, post‐traumatic astrogliosis was much reduced. The Schwann cells transplanted area was invaded by numerous regenerating axons, the vast majority of which were, based on the neurotransmitter (CGRP and SP) profile, originating from dorsal root ganglion. No regeneration of the cortico‐spinal tract as assessed after anterograde tracing or of descending aminergic fibers could be demonstrated. © 1996 Wiley‐Liss, Inc.

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Schwann Cells in Central Regeneration^a

Cited by 15 publications

References 16 publications

Neurotrophic Schwann-cell factors induce neural differentiation of bone marrow stromal cells

Neurotrophic Schwann-cell factors induce neural differentiation of bone marrow stromal cells

Protection and repair of the injured spinal cord: a review of completed, ongoing, and planned clinical trials for acute spinal cord injury

Effects of Schwann cell transplantation in a contusion model of rat spinal cord injury

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Schwann Cells in Central Regenerationa

Cited by 15 publications

References 16 publications

Neurotrophic Schwann-cell factors induce neural differentiation of bone marrow stromal cells

Neurotrophic Schwann-cell factors induce neural differentiation of bone marrow stromal cells

Protection and repair of the injured spinal cord: a review of completed, ongoing, and planned clinical trials for acute spinal cord injury

Effects of Schwann cell transplantation in a contusion model of rat spinal cord injury

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Product

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Schwann Cells in Central Regeneration^a