Chondroitinase ABC promotes functional recovery after spinal cord injury

By E. Bradbury, L. Moon, R. Popat, V. King, G. S. Bennett, Preena Patel, J. Fawcett, S. McMahon. Nature, 2002

2,176 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/4222281cb9fe3031e012d88edb68852bfd3a9d67

How researchers see this paper

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In Cellular and Molecular Neuroscience

1. M. Pekny
2. M. Pekna
3. B. Barres
4. J. Silver
5. J. Gensel
6. A. Tran
7. P. Warren
8. J. Frisén

In Developmental Neuroscience

1. M. Pekny
2. M. Pekna
3. J. Silver
4. J. Frisén
5. Glenn Yiu
6. Zhigang He
7. A. Tran
8. B. Barres

In Pathology and Forensic Medicine

1. J. Gensel
2. David J. Loane
3. Alok Kumar

Citations in the corpus

• Neural tissue engineering: strategies for repair and regeneration. (2003, background): “Treatment of spinal cord injuries with chondroitinase ABC, an enzyme that degrades the side chains of CSPGs, has been associated with improved regeneration (265) and improved functional recovery (266).”
• Long-Distance Growth and Connectivity of Neural Stem Cells After Severe Spinal Cord Injury (2012, positive): “Descending transmission of electrical activity through grafts was assessed by using previously described techniques (Bradbury et al., 2002).”
• Regeneration beyond the glial scar (2004, background): “Intrathecal application of chondroitinase to animals with bilateral dorsal column lesions resulted in degradation of CSPG at the lesion site, and allowed both ascending sensory and descending motor axon regeneration through, and perhaps even slightly past, the lesio”
• Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “Inhibition of chondroitin sulfate proteoglycans produced by oligodendrocyte progenitor cells and astrocytes (27, 28, 130, 212, 254, 269), downregulation of neurocan expression by astrocytes (213), or regional elimination of reactive astrocytes by -aminobutyrate administration (43) were all shown to ”
• Traumatic Spinal Cord Injury: An Overview of Pathophysiology, Models and Acute Injury Mechanisms (2019, background): “The first successful attempt on improving axon outgrowth and/or sprouting by enzymatic degradation of CSPGs using chondroitinase ABC (ChABC) in a rat SCI model was published in 2002 by Bradbury and colleagues (291).”
• A Broader View: Microbial Enzymes and Their Relevance in Industries, Medicine, and Beyond (2013, positive): “The regeneration of injured spinal cord have been demonstrated using chondroitinases, where this enzyme acts by removing the glial scar and thereby accumulating chondroitin sulfate that stops axon growth [99].”
• Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord (2009, background): “Others have shown that chABC can be used in vivo and in vitro to degrade inhibitory proteoglycan substrates and promote axon sprouting and regeneration (Bradbury et al., 2002; Steinmetz et al., 2005).”
• Allodynia limits the usefulness of intraspinal neural stem cell grafts; directed differentiation improves outcome (2005, background): “Instead, overcoming the growth-inhibitory properties of the injured spinal cord milie”
• Glial inhibition of CNS axon regeneration (2006, background): “Intrathecal administration of ChABC following spinal cord injury promoted the regeneration of various axon tracts as well as some recovery of functio”
• Genomic Analysis of Reactive Astrogliosis (2012, background): “For instance, reactive astrocytes can inhibit axon regeneration after CNS injury (McKeon et al., 1991; Bradbury et al., 2002; Fitch and Silver, 2008; Alilain et al., 2011) and can produce proinflammatory cytokines that exacerbate spinal cord injuries (Brambilla et al.”
• The role of the Rho GTPases in neuronal development. (2005, background): “Importantly, the presence of chondroitinase ABC promoted axonal elongation and improved recovery of postsynaptic activity below the lesion site upon electrical stimulation of corticospinal neurons, as well as functional recovery of locomotor and proprioceptive behaviors (Bradbury et al. 2002).”
• CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure. (2008, background): “…also appear to play a key role in creating an environment that is not appropriate for successful long-distance regeneration of adult neurons after injury in vivo, since their modification allows successful regeneration to occur (Bradbury et al., 2002; Houle et al., 2006; Steinmetz et al., 2005).”