Modulation of extracellular matrix components by metalloproteinases and their tissue inhibitors during degeneration and regeneration of rat sural nerve

Gantus, M.A.V.; Nasciutti, Luiz Eurico; Cruz, Cristiane Monteiro da; Persechini, Pedro M.; Martínez, Ana Maria Blanco

doi:10.1016/j.brainres.2006.09.016

Cited by 20 publications

(13 citation statements)

References 39 publications

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“…Successful regeneration is a consequence of well orchestrated interactions between axotomized neurons and non-neuronal cells, especially Schwann cells and macrophages. These interactions are triggered upon injury and initiate a cascade of cellular and molecular reactions including local damage of the blood-nerve-barrier (Weerasuriya and Mizisin 2011;Gray et al 2007;Bouldin et al 1991), degeneration of the distal part of severed axons (Tsao et al 1999;Perry et al 1990;Lubinska 1977), dedifferentiation and proliferation of Schwann cells (LeBlanc and Poduslo 1990), recruitment of hematogenous macrophages LeBlanc and Poduslo 1990), reorganization of the endoneurial extracellular matrix (ECM) (Gantus et al 2006;Tona et al 1993), as well as the release of cytokines, neurotrophins and growth factors (Gordon 2009;Ruohonen et al 2005;Shamash et al 2002). In this way, an axon growthpermissive microenvironment is formed predominantly by non-neuronal adjacent cells, which significantly enhances the intrinsic growth potential of injured peripheral neurons.…”

Section: Introductionmentioning

confidence: 99%

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: Introductionmentioning

confidence: 99%

Extrinsic cellular and molecular mediators of peripheral axonal regeneration

Bosse

2012

Cell Tissue Res

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“…While this scarring can help to reestablish the blood-spinal cord barrier following injury, the cells within the scar prevent neurogenesis by secreting inhibitory molecules. 32 MMP-2 knockout mice show higher prevalence of glial scarring following injury suggesting MMP-2 may also have a beneficial role in improving functional recovery and reducing NP following SCI. Directed inhibition of MMPs may therefore offer an efficient and precise target for the treatment of NP at both early and later phases of presentation.…”

Section: Introductionmentioning

confidence: 99%

Neuropathic pain: role of inflammation, immune response, and ion channel activity in central injury mechanisms

Schomberg¹,

Ahmed²,

Miranpuri³

et al. 2012

ANS

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Neuropathic pain (NP) is a significant and disabling clinical problem with very few therapeutic treatment options available. A major priority is to identify the molecular mechanisms responsible for NP. Although many seemingly relevant pathways have been identified, more research is needed before effective clinical interventions can be produced. Initial insults to the nervous system, such as spinal cord injury (SCI), are often compounded by secondary mechanisms such as inflammation, the immune response, and the changing expression of receptors and ion channels. The consequences of these secondary effects myriad and compound those elicited by the primary injury. Chronic NP syndromes following SCI can greatly complicate the clinical treatment of the primary injury and result in high comorbidity. In this review, we will describe physiological outcomes associated with SCI along with some of the mechanisms known to contribute to chronic NP development.

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“…The regeneration process depends on numerous changes in the extracellular matrix (ECM) 10 occurring concomitantly in both injured nerve and denervated muscles 11–13. These changes require the action of proteolytic zinc‐containing enzymes called matrix metalloproteinases (MMPs), which play a critical role in the ECM reorganization.…”

Section: Introductionmentioning

confidence: 99%