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Article: Gene deletion and pharmacological inhibition of aldose reductase protect against retinal ischemic injury

TitleGene deletion and pharmacological inhibition of aldose reductase protect against retinal ischemic injury
Authors
Keywordsedema
ischemia
Müller cells
neuronal apoptosis
retinal ganglion cell
sorbitol dehydrogenase
Issue Date2007
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexer
Citation
Experimental Eye Research, 2007, v. 85 n. 5, p. 608-616 How to Cite?
AbstractRetinal ischemic injury is common in patients with diabetes, atherosclerosis, hypertension, transient ischemia attack and amaurosis fugax. Previously, signs of ischemic stress, such as pericyte loss, blood-retinal barrier breakdown and neovascularization, which can lead to occlusion of retinal vessels, have been prevented in diabetic db/db mice with aldose reductase (AR) null mutation. To determine the role in retinal ischemic injury of AR and sorbitol dehydrogenase (SDH), the first and second enzymes in the polyol pathway, mice with deletion of AR (AR-/-) or SDH-mutation (SDH-/-), or C57BL/6N mice treated with AR or SDH inhibitors were subjected to transient retinal artery occlusion (2 h of occlusion and 22 h of reperfusion) by the intraluminal suture method. Neuronal loss and edema observed in wildtype (AR+/+) retinas after transient ischemia were prevented in the retinas of AR-/- mice or C57BL/6N mice treated with an AR inhibitor, Fidarestat. Fewer TUNEL-positive cells and smaller accumulations of nitrotyrosine and poly(ADP-ribose) were also observed in the retinas of AR-/- mice. However, SDH-/- mice and C57BL/6N mice treated with SDH inhibitor, CP-470,711, were not protected against ischemia-induced retinal damage. Taken together, AR contributes to retinal ischemic injury through increased edema and free radical accumulation. Therefore, AR inhibition should be considered for the treatment of retinal ischemic injury often observed in diabetic patients. © 2007 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67652
ISSN
2015 Impact Factor: 2.998
2015 SCImago Journal Rankings: 1.218
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, AKHen_HK
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-09-06T05:57:02Z-
dc.date.available2010-09-06T05:57:02Z-
dc.date.issued2007en_HK
dc.identifier.citationExperimental Eye Research, 2007, v. 85 n. 5, p. 608-616en_HK
dc.identifier.issn0014-4835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67652-
dc.description.abstractRetinal ischemic injury is common in patients with diabetes, atherosclerosis, hypertension, transient ischemia attack and amaurosis fugax. Previously, signs of ischemic stress, such as pericyte loss, blood-retinal barrier breakdown and neovascularization, which can lead to occlusion of retinal vessels, have been prevented in diabetic db/db mice with aldose reductase (AR) null mutation. To determine the role in retinal ischemic injury of AR and sorbitol dehydrogenase (SDH), the first and second enzymes in the polyol pathway, mice with deletion of AR (AR-/-) or SDH-mutation (SDH-/-), or C57BL/6N mice treated with AR or SDH inhibitors were subjected to transient retinal artery occlusion (2 h of occlusion and 22 h of reperfusion) by the intraluminal suture method. Neuronal loss and edema observed in wildtype (AR+/+) retinas after transient ischemia were prevented in the retinas of AR-/- mice or C57BL/6N mice treated with an AR inhibitor, Fidarestat. Fewer TUNEL-positive cells and smaller accumulations of nitrotyrosine and poly(ADP-ribose) were also observed in the retinas of AR-/- mice. However, SDH-/- mice and C57BL/6N mice treated with SDH inhibitor, CP-470,711, were not protected against ischemia-induced retinal damage. Taken together, AR contributes to retinal ischemic injury through increased edema and free radical accumulation. Therefore, AR inhibition should be considered for the treatment of retinal ischemic injury often observed in diabetic patients. © 2007 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexeren_HK
dc.relation.ispartofExperimental Eye Researchen_HK
dc.subjectedemaen_HK
dc.subjectischemiaen_HK
dc.subjectMüller cellsen_HK
dc.subjectneuronal apoptosisen_HK
dc.subjectretinal ganglion cellen_HK
dc.subjectsorbitol dehydrogenaseen_HK
dc.subject.meshAldehyde Reductase - antagonists & inhibitors - deficiency - genetics - physiologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshGene Deletionen_HK
dc.subject.meshGlutamic Acid - metabolismen_HK
dc.subject.meshImidazolidines - therapeutic useen_HK
dc.subject.meshL-Iditol 2-Dehydrogenase - antagonists & inhibitors - genetics - physiologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Mutant Strainsen_HK
dc.subject.meshNeuroglia - metabolismen_HK
dc.subject.meshOxidative Stressen_HK
dc.subject.meshPapilledema - enzymology - pathology - prevention & controlen_HK
dc.subject.meshPyrimidines - therapeutic useen_HK
dc.subject.meshReperfusion Injury - enzymology - pathology - prevention & controlen_HK
dc.subject.meshRetinal Diseases - enzymology - pathology - prevention & controlen_HK
dc.subject.meshRetinal Ganglion Cells - pathologyen_HK
dc.titleGene deletion and pharmacological inhibition of aldose reductase protect against retinal ischemic injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-4835&volume=85&spage=608&epage=616&date=2007&atitle=Gene+deletion+and+pharmacological+inhibition+of+aldose+reductase+protect+against+retinal+ischemic+injuryen_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.emailSo, KF: hrmaskf@hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityLo, ACY=rp00425en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.exer.2007.07.013en_HK
dc.identifier.pmid17727843-
dc.identifier.scopuseid_2-s2.0-35549010197en_HK
dc.identifier.hkuros141224en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35549010197&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume85en_HK
dc.identifier.issue5en_HK
dc.identifier.spage608en_HK
dc.identifier.epage616en_HK
dc.identifier.isiWOS:000251444500004-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheung, AKH=7401806412en_HK
dc.identifier.scopusauthoridLo, ACY=7102780640en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK

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