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Conference Paper: Chondroitinase ABC promotes axonal regeneration of Clarke’s neurons beyond the spinal cord injury scar

TitleChondroitinase ABC promotes axonal regeneration of Clarke’s neurons beyond the spinal cord injury scar
Authors
Issue Date2003
PublisherHong Kong Medical Association. The Journal's web site is located at http://www.hkmj.org
Citation
The 8th Medical Research Conference of Department of Medicine (MRC 2003), The University of Hong Kong, Hong Kong, 25-26 January 2003. In Hong Kong Medical Journal, 2003, v. 9 n. S1, p. 72 How to Cite?
AbstractIntroduction: We have previously shown that enzymatic digestion of chondroitin sulfate proteoglycan (CSPG) at the injury scar promotes the axonal regeneration of Clarke’s nucleus (CN) neurons into an peripheral nerve graft after spinal cord hemisection. The present study examined whether digestion of CSPG using chondroitinase ABC promoted the regeneration of CN neurons across the scar into the rostral spinal cord in neonatal and adult rats. Method: Following hemisection of the spinal cord at T11, either vehicle or chondroitinase ABC was applied onto the lesion site. The postoperative survival periods were 2 and 4 weeks. Regenerating CN neurons were retrogradely labeled by Fluoro-Gold injection at spinal cord level C7. Results: In the sham group, there was no regeneration of injured CN neurons in both neonatal and adult rats. Treatment with chondroitinase ABC in neonates resulted in 11.8% and 8.3% of the injured CN neurons regenerated into the rostral spinal cord, 2 and 4 weeks respectively. In adults, there were 9.4% and 12.3%, 2 and 4 weeks respectively, of the injured CN neurons regenerated their axons to the rostral spinal cord. After chondroitinase ABC treatment, the immunoreactivity for CSPG was dramatically decreased around the lesion site in both neonatal and adult animals. Conclusion: Our results show that degradation of CSPG with chondroitinase ABC can promote the axonal regeneration in the spinal cord. These results further support the hypothesis that CSPG is inhibitory to the regeneration of neurons in the spinal cord after traumatic injury. Acknowledgement: This work was supported by grants from the Hong Kong Research Grants Council and the University of Hong Kong.
Persistent Identifierhttp://hdl.handle.net/10722/95422
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorYick, LWen_HK
dc.contributor.authorCheung, PTen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-09-25T16:01:46Z-
dc.date.available2010-09-25T16:01:46Z-
dc.date.issued2003en_HK
dc.identifier.citationThe 8th Medical Research Conference of Department of Medicine (MRC 2003), The University of Hong Kong, Hong Kong, 25-26 January 2003. In Hong Kong Medical Journal, 2003, v. 9 n. S1, p. 72en_HK
dc.identifier.issn1024-2708en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95422-
dc.description.abstractIntroduction: We have previously shown that enzymatic digestion of chondroitin sulfate proteoglycan (CSPG) at the injury scar promotes the axonal regeneration of Clarke’s nucleus (CN) neurons into an peripheral nerve graft after spinal cord hemisection. The present study examined whether digestion of CSPG using chondroitinase ABC promoted the regeneration of CN neurons across the scar into the rostral spinal cord in neonatal and adult rats. Method: Following hemisection of the spinal cord at T11, either vehicle or chondroitinase ABC was applied onto the lesion site. The postoperative survival periods were 2 and 4 weeks. Regenerating CN neurons were retrogradely labeled by Fluoro-Gold injection at spinal cord level C7. Results: In the sham group, there was no regeneration of injured CN neurons in both neonatal and adult rats. Treatment with chondroitinase ABC in neonates resulted in 11.8% and 8.3% of the injured CN neurons regenerated into the rostral spinal cord, 2 and 4 weeks respectively. In adults, there were 9.4% and 12.3%, 2 and 4 weeks respectively, of the injured CN neurons regenerated their axons to the rostral spinal cord. After chondroitinase ABC treatment, the immunoreactivity for CSPG was dramatically decreased around the lesion site in both neonatal and adult animals. Conclusion: Our results show that degradation of CSPG with chondroitinase ABC can promote the axonal regeneration in the spinal cord. These results further support the hypothesis that CSPG is inhibitory to the regeneration of neurons in the spinal cord after traumatic injury. Acknowledgement: This work was supported by grants from the Hong Kong Research Grants Council and the University of Hong Kong.-
dc.languageengen_HK
dc.publisherHong Kong Medical Association. The Journal's web site is located at http://www.hkmj.orgen_HK
dc.relation.ispartofHong Kong Medical Journalen_HK
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Medical Association.en_HK
dc.titleChondroitinase ABC promotes axonal regeneration of Clarke’s neurons beyond the spinal cord injury scaren_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1024-2708&volume=9 supplement&spage=72&epage=&date=2003&atitle=Chondroitinase+ABC+promotes+axonal+regeneratiion+of+Clarke%27s+neurons+beyond+the+spinal+cord+injury+scaren_HK
dc.identifier.emailYick, LW: yickkevinhk@yahoo.comen_HK
dc.identifier.emailCheung, PT: ptcheung@hkucc.hku.hken_HK
dc.identifier.emailSo, KF: hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailWu, W: wtwu@hkucc.hku.hken_HK
dc.identifier.authorityCheung, PT=rp00351en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.identifier.hkuros141348en_HK
dc.identifier.volume9en_HK
dc.identifier.spage72en_HK

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