2011
DOI: 10.1016/j.expneurol.2011.05.002
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Chondroitinase treatment following spinal contusion injury increases migration of oligodendrocyte progenitor cells

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Cited by 85 publications
(79 citation statements)
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References 32 publications
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“…Kwon et al [2001]) were tested in a rodent contusion model of the spinal cord. Briefly, a moderate contusion injury was generated using an impactor rod drop with an NYU impactor [Siebert et al, 2011] in the T9-T11 region of the rat spinal cord. Immediately after the injury, 3 μl of a 20-mg/ml suspension of nanoparticles were injected into the rostral and caudal edges of the lesion along the midline using a microinjection apparatus.…”
Section: Use Of Chabc-releasing Nanoparticles Within a Rodent Model Omentioning
confidence: 99%
See 1 more Smart Citation
“…Kwon et al [2001]) were tested in a rodent contusion model of the spinal cord. Briefly, a moderate contusion injury was generated using an impactor rod drop with an NYU impactor [Siebert et al, 2011] in the T9-T11 region of the rat spinal cord. Immediately after the injury, 3 μl of a 20-mg/ml suspension of nanoparticles were injected into the rostral and caudal edges of the lesion along the midline using a microinjection apparatus.…”
Section: Use Of Chabc-releasing Nanoparticles Within a Rodent Model Omentioning
confidence: 99%
“…The animals were sacrificed at various times postinjury to evaluate the extent of chABC release from nanospheres and proteoglycan digestion in vivo. The in vivo release of chABC from nanoparticles was detected by immunohistochemistry for the CSPGs in their native form or cleaved forms of CSPGs using the antibody CS56 (identifies undigested CSPG) or 2B6 (identifies chABC-digested CSPGs) [Siebert et al, 2011]. The lesion site can be outlined in spinal cord sections by immunostaining for GFAP (glial fibrillary acidic protein), which identifies the reactive astrocytes surrounding the lesion site.…”
Section: Use Of Chabc-releasing Nanoparticles Within a Rodent Model Omentioning
confidence: 99%
“…Because it is known that CSPGs also inhibit axonal regeneration, and perturbation of CSPGs promotes axonal sprouting [128,129], it could be argued that increased remyelination after xyloside treatment is a consequence of increased axonal targets for new sheath development and not per se true remyelination. However, at least in spinal cord injury models, the kinetics of axonal sprouting and OPC invasion are discordant, suggesting that the 2 events are independent and CSPG disruption could indeed directly promote remyelination [130].…”
Section: Extracellular Matrix Moleculesmentioning
confidence: 99%
“…Alternatively, the receptors that bind CSPGs, including protein tyrosine phosphatase-σ, leukocyte common antigen-related phosphatase, or Nogo-66 receptor 1 and 3, could potentially be targets for the development of antagonistic inhibitors [133][134][135]. It is important to note that the majority of work investigating CSPG-mediated inhibition has been focused on growth of neurites after traumatic injuries, and inhibition of OPCs by CSPGs has only recently been put in the spotlight [126,127,130]. Whether similar or different mechanisms mediate CSPG inhibition of neurons versus OPCs awaits further study.…”
Section: Extracellular Matrix Moleculesmentioning
confidence: 99%
“…Trabalhos mais atuais apostam na resolução da cicatriz da glia associadas às terapias com células-tronco para o tratamento da lesão medular crônica (IKEGAMI et al, 2005;SIEBERT et al, 2011 …”
Section: Discussionunclassified