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Article: CNTF promotes survival of retinal ganglion cells after induction of ocular hypertension in rats: The possible involvement of STAT3 pathway

TitleCNTF promotes survival of retinal ganglion cells after induction of ocular hypertension in rats: The possible involvement of STAT3 pathway
Authors
Issue Date2004
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/EJN
Citation
European Journal Of Neuroscience, 2004, v. 19 n. 2, p. 265-272 How to Cite?
AbstractWe examined the neuroprotective effect of ciliary neurotrophic factor (CNTF) on retinal ganglion cells (RGCs) in a rat glaucoma model with increased intraocular pressure (IOP) and studied the CNTF-mediated activation of Janus kinase/signal transducer and activator of transcription (JAK-STAT) pathway. Elevated IOP was induced by laser photocoagulation of the episcleral and limbal veins. The survival of RGCs was studied using Fluoro-Gold labelled in ocular hypertensive eyes with or without CNTF intravitreal injection. Immunochemical staining and immunoblot analysis for CNTF and phosphorylated STAT3 (pSTAT3) were performed. There was a significant and progressive loss of RGCs in the retinas following the induction of elevated IOP. A single intravitreal injection of 2 μg in 2 μL CNTF significantly protected RGCs up to 4 weeks. pSTAT3 was only transiently expressed in ocular hypertensive eyes. However, in eyes treated with CNTF, pSTAT3 was observed up to 2 weeks after the induction of elevated IOP. In ocular hypertensive eyes, CNTF-positive cells were found in the inner nuclear layer (INL), and there was a transient increase in the pSTAT3 cells in the ganglion cell layer and INL. Immunoblots showed that STAT3 was transiently phosphorylated after IOP increase, but with an injection of CNTF, pSTAT3 protein was observed up to 2 weeks after hypertensive glaucoma induction. Laser-induced chronic ocular hypertension in rats resulted in the death of RGCs and a transient activation of STAT3 in the retina. Intravitreal injection of CNTF showed a significant protection of RGCs, and the JAK-STAT signalling could be one of the important pathways that underlie the mechanism of CNTF neuroprotection in this rat glaucoma model.
Persistent Identifierhttp://hdl.handle.net/10722/67694
ISSN
2015 Impact Factor: 2.975
2015 SCImago Journal Rankings: 2.130
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJi, JZen_HK
dc.contributor.authorElyaman, Wen_HK
dc.contributor.authorYip, HKen_HK
dc.contributor.authorLee, VWHen_HK
dc.contributor.authorYick, LWen_HK
dc.contributor.authorHugon, Jen_HK
dc.contributor.authorSo, KFen_HK
dc.date.accessioned2010-09-06T05:57:25Z-
dc.date.available2010-09-06T05:57:25Z-
dc.date.issued2004en_HK
dc.identifier.citationEuropean Journal Of Neuroscience, 2004, v. 19 n. 2, p. 265-272en_HK
dc.identifier.issn0953-816Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/67694-
dc.description.abstractWe examined the neuroprotective effect of ciliary neurotrophic factor (CNTF) on retinal ganglion cells (RGCs) in a rat glaucoma model with increased intraocular pressure (IOP) and studied the CNTF-mediated activation of Janus kinase/signal transducer and activator of transcription (JAK-STAT) pathway. Elevated IOP was induced by laser photocoagulation of the episcleral and limbal veins. The survival of RGCs was studied using Fluoro-Gold labelled in ocular hypertensive eyes with or without CNTF intravitreal injection. Immunochemical staining and immunoblot analysis for CNTF and phosphorylated STAT3 (pSTAT3) were performed. There was a significant and progressive loss of RGCs in the retinas following the induction of elevated IOP. A single intravitreal injection of 2 μg in 2 μL CNTF significantly protected RGCs up to 4 weeks. pSTAT3 was only transiently expressed in ocular hypertensive eyes. However, in eyes treated with CNTF, pSTAT3 was observed up to 2 weeks after the induction of elevated IOP. In ocular hypertensive eyes, CNTF-positive cells were found in the inner nuclear layer (INL), and there was a transient increase in the pSTAT3 cells in the ganglion cell layer and INL. Immunoblots showed that STAT3 was transiently phosphorylated after IOP increase, but with an injection of CNTF, pSTAT3 protein was observed up to 2 weeks after hypertensive glaucoma induction. Laser-induced chronic ocular hypertension in rats resulted in the death of RGCs and a transient activation of STAT3 in the retina. Intravitreal injection of CNTF showed a significant protection of RGCs, and the JAK-STAT signalling could be one of the important pathways that underlie the mechanism of CNTF neuroprotection in this rat glaucoma model.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/EJNen_HK
dc.relation.ispartofEuropean Journal of Neuroscienceen_HK
dc.rightsEuropean Journal of Neuroscience. Copyright © Blackwell Publishing Ltd.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Survival - physiologyen_HK
dc.subject.meshCiliary Neurotrophic Factor - physiology - therapeutic useen_HK
dc.subject.meshDNA-Binding Proteins - physiologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshNeuroprotective Agents - therapeutic useen_HK
dc.subject.meshOcular Hypertension - drug therapy - metabolism - pathologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshRetinal Ganglion Cells - cytology - metabolism - pathologyen_HK
dc.subject.meshSTAT3 Transcription Factoren_HK
dc.subject.meshSignal Transduction - drug effects - physiologyen_HK
dc.subject.meshTrans-Activators - physiologyen_HK
dc.titleCNTF promotes survival of retinal ganglion cells after induction of ocular hypertension in rats: The possible involvement of STAT3 pathwayen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0953-816X&volume=19&spage=265&epage=272&date=2004&atitle=CNTF+promotes+survival+of+retinal+ganglion+cells+after+induction+of+ocular+hypertension+in+rats:+the+possible+involvement+of+STAT3+pathwayen_HK
dc.identifier.emailYip, HK:hkfyip@hku.hken_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.authorityYip, HK=rp00285en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.0953-816X.2003.03107.xen_HK
dc.identifier.pmid14725620-
dc.identifier.scopuseid_2-s2.0-0842308889en_HK
dc.identifier.hkuros85897en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0842308889&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume19en_HK
dc.identifier.issue2en_HK
dc.identifier.spage265en_HK
dc.identifier.epage272en_HK
dc.identifier.isiWOS:000188224800005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridJi, JZ=7201362425en_HK
dc.identifier.scopusauthoridElyaman, W=6603236614en_HK
dc.identifier.scopusauthoridYip, HK=7101980864en_HK
dc.identifier.scopusauthoridLee, VWH=7402507569en_HK
dc.identifier.scopusauthoridYick, LW=6603414804en_HK
dc.identifier.scopusauthoridHugon, J=7103202992en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK

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