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Article: Aldose reductase deficiency reduced vascular changes in neonatal mouse retina in oxygen-induced retinopathy

TitleAldose reductase deficiency reduced vascular changes in neonatal mouse retina in oxygen-induced retinopathy
Authors
Issue Date2012
PublisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.org
Citation
Investigative Ophthalmology & Visual Science, 2012, v. 53 n. 9, p. 5698-5712 How to Cite?
Abstract
PURPOSE: Retinal neovascularization is the major pathologic process in many ocular diseases and is associated with oxidative stress. Deficiency of aldose reductase (AR), the first enzyme in the polyol pathway for glucose metabolism, has been shown to reduce oxidative stress and blood vessel leakage. The present study aimed to investigate the effect of AR deficiency on retinal neovascularization in a murine oxygen-induced retinopathy (OIR) model. METHODS: Seven-day-old wild-type (WT) and AR-deficient (AR(-/-)) mice were exposed to 75% oxygen for 5 days and then returned to room air. Vascular obliteration, neovascularization, and blood vessel leakage were analyzed and compared. Immunohistochemistry for AR, nitrotyrosine (NT), poly(ADP-ribose) (PAR), glial fibrillary acidic protein (GFAP), and Iba-1, as well as Western blots for vascular endothelial growth factor (VEGF), phospho-Erk (p-Erk), phospho-Akt (p-Akt), and phospho-IkappaB (p-IkappaB) were performed. RESULTS: Compared with WT OIR retinae, AR(-/-) OIR retinae displayed significantly smaller central retinal vaso-obliterated area, less neovascularization, and reduced blood vessel leakage. Significantly reduced oxidative stress and glial responses were also observed in AR(-/-) OIR retinae. Moreover, reduced microglial response in the avascular area but increased microglial responses in the neovascular area were found with AR deficiency. Furthermore, expression levels of VEGF, p-Erk, p-Akt, and p-IkappaB were significantly reduced in AR(-/-) OIR retinae. CONCLUSIONS: Our observations indicated that AR deficiency reduced retinal vascular changes in the mouse model of OIR, indicating that AR can be a potential therapeutic target in ischemia-induced retinopathy.
Persistent Identifierhttp://hdl.handle.net/10722/166833
ISSN
2013 Impact Factor: 3.661
2013 SCImago Journal Rankings: 2.185
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFu, ZJen_US
dc.contributor.authorLi, SYen_US
dc.contributor.authorKociok, Nen_US
dc.contributor.authorWong, Den_US
dc.contributor.authorChung, SKen_US
dc.contributor.authorLo, ACYen_US
dc.date.accessioned2012-09-20T08:50:38Z-
dc.date.available2012-09-20T08:50:38Z-
dc.date.issued2012en_US
dc.identifier.citationInvestigative Ophthalmology & Visual Science, 2012, v. 53 n. 9, p. 5698-5712en_US
dc.identifier.issn0146-0404-
dc.identifier.urihttp://hdl.handle.net/10722/166833-
dc.description.abstractPURPOSE: Retinal neovascularization is the major pathologic process in many ocular diseases and is associated with oxidative stress. Deficiency of aldose reductase (AR), the first enzyme in the polyol pathway for glucose metabolism, has been shown to reduce oxidative stress and blood vessel leakage. The present study aimed to investigate the effect of AR deficiency on retinal neovascularization in a murine oxygen-induced retinopathy (OIR) model. METHODS: Seven-day-old wild-type (WT) and AR-deficient (AR(-/-)) mice were exposed to 75% oxygen for 5 days and then returned to room air. Vascular obliteration, neovascularization, and blood vessel leakage were analyzed and compared. Immunohistochemistry for AR, nitrotyrosine (NT), poly(ADP-ribose) (PAR), glial fibrillary acidic protein (GFAP), and Iba-1, as well as Western blots for vascular endothelial growth factor (VEGF), phospho-Erk (p-Erk), phospho-Akt (p-Akt), and phospho-IkappaB (p-IkappaB) were performed. RESULTS: Compared with WT OIR retinae, AR(-/-) OIR retinae displayed significantly smaller central retinal vaso-obliterated area, less neovascularization, and reduced blood vessel leakage. Significantly reduced oxidative stress and glial responses were also observed in AR(-/-) OIR retinae. Moreover, reduced microglial response in the avascular area but increased microglial responses in the neovascular area were found with AR deficiency. Furthermore, expression levels of VEGF, p-Erk, p-Akt, and p-IkappaB were significantly reduced in AR(-/-) OIR retinae. CONCLUSIONS: Our observations indicated that AR deficiency reduced retinal vascular changes in the mouse model of OIR, indicating that AR can be a potential therapeutic target in ischemia-induced retinopathy.-
dc.languageengen_US
dc.publisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.org-
dc.relation.ispartofInvestigative Ophthalmology & Visual Scienceen_US
dc.subject.meshAldehyde Reductase - deficiency-
dc.subject.meshAnimals, Newborn-
dc.subject.meshDisease Models, Animal-
dc.subject.meshRetinal Neovascularization - enzymology - pathology - prevention and control-
dc.subject.meshRetinopathy of Prematurity - enzymology - pathology - prevention and control-
dc.titleAldose reductase deficiency reduced vascular changes in neonatal mouse retina in oxygen-induced retinopathyen_US
dc.typeArticleen_US
dc.identifier.emailLi, SY: sukyeeli@hku.hken_US
dc.identifier.emailWong, D: shdwong@hku.hken_US
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_US
dc.identifier.emailLo, ACY: amylo@hku.hken_US
dc.identifier.authorityWong, DSH=rp00516en_US
dc.identifier.authorityChung, SK=rp00381en_US
dc.identifier.authorityLo, ACY=rp00425en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1167/iovs.12-10122-
dc.identifier.pmid22836764-
dc.identifier.hkuros208513en_US
dc.identifier.volume53en_US
dc.identifier.issue9-
dc.identifier.spage5698en_US
dc.identifier.epage5712en_US
dc.identifier.isiWOS:000308695400074-
dc.publisher.placeUnited States-

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