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Conference Paper: Heparanase upregulation in astrocytes and macrophages recruited to the injured spinal cord

TitleHeparanase upregulation in astrocytes and macrophages recruited to the injured spinal cord
Authors
Issue Date2007
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neures
Citation
The 30th Annual Meeting of the Japan Neuroscience Society, Yokohama, Japan, 10–12 September 2007. In Neuroscience Research, 2007, v. 58 n. S1, p. S145 How to Cite?
AbstractMammalian heparanase (Hpa1) is a heparan sulfate-cleaving endo-glucuronidase exploited by inflammatory and cancer cells to invade connective tissues. We hypothesize Hpa1 involvement also in the recruitment of reactive astrocytes and macrophages to the injured spinal cord. To test this, spinal cords of adult rats were hemisected at T8. Q-PCR for Hpa1 mRNA in the cord at T7-9 indicated initial (3 dpi) decrease followed by progressive increase to levels in excess of that in the normal cord by 14 dpi. Combined in situ hybridization for Hpa1 mRNA and immunocytochemistry for cell markers indicated increased Hpa1 expression in GFAP+ astrocytes and ED-1+ macrophages in the lesion by 7–14 dpi. Upregulated Hpa1 expression was also observed in astrocytes that invaded the scratched area in an in vitro model. Taken together, our results indicated upregulated expression of Hpa1 in astrocytes and macrophages that were recruited to the injury. Research funds: CRCG10204997 & 10205634 to DKYS
Persistent Identifierhttp://hdl.handle.net/10722/96684
ISSN
2023 Impact Factor: 2.4
2023 SCImago Journal Rankings: 0.811
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorChau, CHen_HK
dc.contributor.authorChan, YSen_HK
dc.contributor.authorShum, DKYen_HK
dc.date.accessioned2010-09-25T16:41:29Z-
dc.date.available2010-09-25T16:41:29Z-
dc.date.issued2007en_HK
dc.identifier.citationThe 30th Annual Meeting of the Japan Neuroscience Society, Yokohama, Japan, 10–12 September 2007. In Neuroscience Research, 2007, v. 58 n. S1, p. S145-
dc.identifier.issn0168-0102-
dc.identifier.urihttp://hdl.handle.net/10722/96684-
dc.description.abstractMammalian heparanase (Hpa1) is a heparan sulfate-cleaving endo-glucuronidase exploited by inflammatory and cancer cells to invade connective tissues. We hypothesize Hpa1 involvement also in the recruitment of reactive astrocytes and macrophages to the injured spinal cord. To test this, spinal cords of adult rats were hemisected at T8. Q-PCR for Hpa1 mRNA in the cord at T7-9 indicated initial (3 dpi) decrease followed by progressive increase to levels in excess of that in the normal cord by 14 dpi. Combined in situ hybridization for Hpa1 mRNA and immunocytochemistry for cell markers indicated increased Hpa1 expression in GFAP+ astrocytes and ED-1+ macrophages in the lesion by 7–14 dpi. Upregulated Hpa1 expression was also observed in astrocytes that invaded the scratched area in an in vitro model. Taken together, our results indicated upregulated expression of Hpa1 in astrocytes and macrophages that were recruited to the injury. Research funds: CRCG10204997 & 10205634 to DKYS-
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neures-
dc.relation.ispartofNeuroscience Researchen_HK
dc.titleHeparanase upregulation in astrocytes and macrophages recruited to the injured spinal corden_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChau, CH: mchchau@hkucc.hku.hken_HK
dc.identifier.emailLai, CH: chlaib@HKUSUA.hku.hken_HK
dc.identifier.emailChan, YS: yschan@hkucc.hku.hken_HK
dc.identifier.emailShum, DKY: shumdkhk@hkucc.hku.hken_HK
dc.identifier.authorityChau, CH=rp00398en_HK
dc.identifier.authorityLai, CH=rp00396en_HK
dc.identifier.authorityChan, YS=rp00318en_HK
dc.identifier.authorityShum, DKY=rp00321en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neures.2007.06.1421-
dc.identifier.hkuros149739en_HK
dc.identifier.isiWOS:000249272800853-
dc.identifier.issnl0168-0102-

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