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Article: Enhanced survival of melanopsin-expressing retinal ganglion cells after injury is associated with the PI3 K/Akt pathway

TitleEnhanced survival of melanopsin-expressing retinal ganglion cells after injury is associated with the PI3 K/Akt pathway
Authors
Issue Date2008
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0272-4340
Citation
Cellular And Molecular Neurobiology, 2008, v. 28 n. 8, p. 1095-1107 How to Cite?
AbstractIn the present study, we studied the factors that contribute to the injury-resistant property of melanopsin-expressing retinal ganglion cells (mRGCs). Since phosphatidylinositol-3 kinase (PI3 K)/Akt signaling pathway is one of the well-known pathways for neuronal cell survival, we investigated the survival of mRGCs by applying the PI3 K/Akt specific inhibitors after injury. Two injury models, unilateral optic nerve transection and ocular hypertension, were adopted using Sprague-Dawley rats. Inhibitors of PI3 K/Akt were injected intravitreally following injuries to inhibit the PI3 K/Akt signaling pathway. Retinas were dissected after designated survival time, immunohistochemistry was carried out to visualize the mRGCs using melanopsin antibody and the number of mRGCs was counted. Co-expression of melanopsin and phospho-Akt (pAkt) was also examined. Compared to the survival of non-melanopsin-expressing RGCs, mRGCs showed a marked resistance to injury and co-expressed pAkt. Application of PI3 K/Akt inhibitors decreased the survival of mRGCs after injury. Our previous study has shown that mRGC are less susceptible to injury following the induction of ocular hypertension. In this study, we report that mRGCs were injury-resistant to a more severe type of injury, the optic nerve transection. More importantly, the PI3 K/Akt pathway was found to play a role in maintaining the survival of mRGCs after injury. © 2008 Springer Science+Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/67655
ISSN
2015 Impact Factor: 2.328
2015 SCImago Journal Rankings: 1.005
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Charitable Foundation
Hong Kong Polytechnic UniversityBQ-867
Funding Information:

We would like to thank Mr. Tak-Ho Chu and Dr. Bing Hu for their stimulating discussion and comment on the manuscript. Our study was supported by the donations from the Hong Kong Charitable Foundation, and Ms. Annie Tsao Wen Wei and the Competitive Earmarked Research Grant (BQ-867) of The Hong Kong Polytechnic University.

References

 

DC FieldValueLanguage
dc.contributor.authorLi, SYen_HK
dc.contributor.authorYau, SYen_HK
dc.contributor.authorChen, BYen_HK
dc.contributor.authorTay, DKen_HK
dc.contributor.authorLee, VWHen_HK
dc.contributor.authorPu, MLen_HK
dc.contributor.authorChan, HHLen_HK
dc.contributor.authorSo, KFen_HK
dc.date.accessioned2010-09-06T05:57:04Z-
dc.date.available2010-09-06T05:57:04Z-
dc.date.issued2008en_HK
dc.identifier.citationCellular And Molecular Neurobiology, 2008, v. 28 n. 8, p. 1095-1107en_HK
dc.identifier.issn0272-4340en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67655-
dc.description.abstractIn the present study, we studied the factors that contribute to the injury-resistant property of melanopsin-expressing retinal ganglion cells (mRGCs). Since phosphatidylinositol-3 kinase (PI3 K)/Akt signaling pathway is one of the well-known pathways for neuronal cell survival, we investigated the survival of mRGCs by applying the PI3 K/Akt specific inhibitors after injury. Two injury models, unilateral optic nerve transection and ocular hypertension, were adopted using Sprague-Dawley rats. Inhibitors of PI3 K/Akt were injected intravitreally following injuries to inhibit the PI3 K/Akt signaling pathway. Retinas were dissected after designated survival time, immunohistochemistry was carried out to visualize the mRGCs using melanopsin antibody and the number of mRGCs was counted. Co-expression of melanopsin and phospho-Akt (pAkt) was also examined. Compared to the survival of non-melanopsin-expressing RGCs, mRGCs showed a marked resistance to injury and co-expressed pAkt. Application of PI3 K/Akt inhibitors decreased the survival of mRGCs after injury. Our previous study has shown that mRGC are less susceptible to injury following the induction of ocular hypertension. In this study, we report that mRGCs were injury-resistant to a more severe type of injury, the optic nerve transection. More importantly, the PI3 K/Akt pathway was found to play a role in maintaining the survival of mRGCs after injury. © 2008 Springer Science+Business Media, LLC.en_HK
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0272-4340en_HK
dc.relation.ispartofCellular and Molecular Neurobiologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAxotomyen_HK
dc.subject.meshCell Death - drug effectsen_HK
dc.subject.meshCell Survival - drug effectsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshInjectionsen_HK
dc.subject.meshOptic Nerve Injuriesen_HK
dc.subject.meshPhosphatidylinositol 3-Kinases - antagonists & inhibitors - metabolismen_HK
dc.subject.meshPhosphoproteins - metabolismen_HK
dc.subject.meshProtein Kinase Inhibitors - administration & dosage - pharmacologyen_HK
dc.subject.meshProto-Oncogene Proteins c-akt - antagonists & inhibitors - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshRetinal Ganglion Cells - drug effects - enzymology - pathologyen_HK
dc.subject.meshRod Opsins - metabolismen_HK
dc.subject.meshSuperior Colliculi - drug effects - enzymology - pathologyen_HK
dc.titleEnhanced survival of melanopsin-expressing retinal ganglion cells after injury is associated with the PI3 K/Akt pathwayen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0272-4340&volume=28&spage=1095&epage=1107&date=2008&atitle=Enhanced+Survival+of+Melanopsin-expressing+Retinal+Ganglion+Cells+After+Injury+is+Associated+with+the+PI3+K/Akt+Pathwayen_HK
dc.identifier.emailTay, DK:dkctay@hkucc.hku.hken_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.authorityTay, DK=rp00336en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10571-008-9286-xen_HK
dc.identifier.pmid18512147-
dc.identifier.scopuseid_2-s2.0-57449102421en_HK
dc.identifier.hkuros142253en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-57449102421&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume28en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1095en_HK
dc.identifier.epage1107en_HK
dc.identifier.isiWOS:000261329500007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, SY=24329630700en_HK
dc.identifier.scopusauthoridYau, SY=24330296200en_HK
dc.identifier.scopusauthoridChen, BY=14051424300en_HK
dc.identifier.scopusauthoridTay, DK=7006796825en_HK
dc.identifier.scopusauthoridLee, VWH=7402507569en_HK
dc.identifier.scopusauthoridPu, ML=16073321400en_HK
dc.identifier.scopusauthoridChan, HHL=24774420300en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK

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