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Article: Aldose reductase deficiency prevents diabetes-induced blood-retinal barrier breakdown, apoptosis, and glial reactivation in the retina of db/db mice

TitleAldose reductase deficiency prevents diabetes-induced blood-retinal barrier breakdown, apoptosis, and glial reactivation in the retina of db/db mice
Authors
Issue Date2005
PublisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/
Citation
Diabetes, 2005, v. 54 n. 11, p. 3119-3125 How to Cite?
AbstractIn 15-month-old db/db mice, signs of diabetic retinopathy, including blood-retinal barrier breakdown, loss of pericytes, neuro-retinal apoptosis, glial reactivation, and proliferation of blood vessels, were evident. These changes in the diabetic retina were associated with increased expression of aldose reductase (AR). To further understand the role of AR in the pathogenesis of diabetic retinopathy, we generated db/db mice with an AR null mutation (AR -/- db/db). AR deficiency led to fewer retinal blood vessels with IgG leakage, suggesting that AR may contribute to blood-retinal barrier breakdown. AR deficiency also prevented diabetes-induced reduction of platelet/endothelial cell adhesion molecule-1 expression and increased expression of vascular endothelial growth factor, which may have contributed to blood-retinal barrier breakdown. In addition, long-term diabetes-induced neuro-retinal stress and apoptosis and proliferation of blood vessels were less prominent in AR -/- db/db mice. These findings indicate that AR is responsible for the early events in the pathogenesis of diabetic retinopathy, leading to a cascade of retinal lesions, including blood-retinal barrier breakdown, loss of pericytes, neuro-retinal apoptosis, glial reactivation, and neovascularization. © 2005 by the American Diabetes Association.
Persistent Identifierhttp://hdl.handle.net/10722/146630
ISSN
2015 Impact Factor: 8.784
2015 SCImago Journal Rankings: 5.185
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, AKHen_HK
dc.contributor.authorFung, MKLen_HK
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorLam, TTLen_HK
dc.contributor.authorKwok, FSen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2012-05-08T03:21:23Z-
dc.date.available2012-05-08T03:21:23Z-
dc.date.issued2005en_HK
dc.identifier.citationDiabetes, 2005, v. 54 n. 11, p. 3119-3125en_HK
dc.identifier.issn0012-1797en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146630-
dc.description.abstractIn 15-month-old db/db mice, signs of diabetic retinopathy, including blood-retinal barrier breakdown, loss of pericytes, neuro-retinal apoptosis, glial reactivation, and proliferation of blood vessels, were evident. These changes in the diabetic retina were associated with increased expression of aldose reductase (AR). To further understand the role of AR in the pathogenesis of diabetic retinopathy, we generated db/db mice with an AR null mutation (AR -/- db/db). AR deficiency led to fewer retinal blood vessels with IgG leakage, suggesting that AR may contribute to blood-retinal barrier breakdown. AR deficiency also prevented diabetes-induced reduction of platelet/endothelial cell adhesion molecule-1 expression and increased expression of vascular endothelial growth factor, which may have contributed to blood-retinal barrier breakdown. In addition, long-term diabetes-induced neuro-retinal stress and apoptosis and proliferation of blood vessels were less prominent in AR -/- db/db mice. These findings indicate that AR is responsible for the early events in the pathogenesis of diabetic retinopathy, leading to a cascade of retinal lesions, including blood-retinal barrier breakdown, loss of pericytes, neuro-retinal apoptosis, glial reactivation, and neovascularization. © 2005 by the American Diabetes Association.en_HK
dc.languageengen_US
dc.publisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/en_HK
dc.relation.ispartofDiabetesen_HK
dc.subject.meshAldehyde Reductase - Deficiency - Geneticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntigens, Cd31 - Geneticsen_US
dc.subject.meshApoptosis - Physiologyen_US
dc.subject.meshBlood-Retinal Barrier - Physiopathologyen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshDiabetes Mellitus - Genetics - Physiopathologyen_US
dc.subject.meshGene Deletionen_US
dc.subject.meshGene Expression Regulation, Enzymologicen_US
dc.subject.meshMiceen_US
dc.subject.meshNeurogliaen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshRetina - Cytology - Enzymologyen_US
dc.subject.meshVascular Endothelial Growth Factor A - Geneticsen_US
dc.titleAldose reductase deficiency prevents diabetes-induced blood-retinal barrier breakdown, apoptosis, and glial reactivation in the retina of db/db miceen_HK
dc.typeArticleen_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.emailKwok, FS: 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.authorityKwok, FS=rp00329en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.2337/diabetes.54.11.3119en_HK
dc.identifier.pmid16249434-
dc.identifier.scopuseid_2-s2.0-33644663628en_HK
dc.identifier.hkuros113583-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33644663628&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume54en_HK
dc.identifier.issue11en_HK
dc.identifier.spage3119en_HK
dc.identifier.epage3125en_HK
dc.identifier.isiWOS:000233023100008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, AKH=7401806412en_HK
dc.identifier.scopusauthoridFung, MKL=8718040400en_HK
dc.identifier.scopusauthoridLo, ACY=7102780640en_HK
dc.identifier.scopusauthoridLam, TTL=8915077700en_HK
dc.identifier.scopusauthoridKwok, FS=34668391300en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK

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