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Article: Aldose reductase deficiency reduced vascular changes in neonatal mouse retina in oxygen-induced retinopathy
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TitleAldose reductase deficiency reduced vascular changes in neonatal mouse retina in oxygen-induced retinopathy
 
AuthorsFu, ZJ
Li, SY
Kociok, N
Wong, D
Chung, SK
Lo, ACY
 
Issue Date2012
 
PublisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.org
 
CitationInvestigative Ophthalmology & Visual Science, 2012, v. 53 n. 9, p. 5698-5712 [How to Cite?]
DOI: http://dx.doi.org/10.1167/iovs.12-10122
 
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.
 
ISSN0146-0404
2013 Impact Factor: 3.661
2013 SCImago Journal Rankings: 2.185
 
DOIhttp://dx.doi.org/10.1167/iovs.12-10122
 
DC FieldValue
dc.contributor.authorFu, ZJ
 
dc.contributor.authorLi, SY
 
dc.contributor.authorKociok, N
 
dc.contributor.authorWong, D
 
dc.contributor.authorChung, SK
 
dc.contributor.authorLo, ACY
 
dc.date.accessioned2012-09-20T08:50:38Z
 
dc.date.available2012-09-20T08:50:38Z
 
dc.date.issued2012
 
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.description.naturelink_to_OA_fulltext
 
dc.identifier.citationInvestigative Ophthalmology & Visual Science, 2012, v. 53 n. 9, p. 5698-5712 [How to Cite?]
DOI: http://dx.doi.org/10.1167/iovs.12-10122
 
dc.identifier.doihttp://dx.doi.org/10.1167/iovs.12-10122
 
dc.identifier.epage5712
 
dc.identifier.hkuros208513
 
dc.identifier.issn0146-0404
2013 Impact Factor: 3.661
2013 SCImago Journal Rankings: 2.185
 
dc.identifier.issue9
 
dc.identifier.pmid22836764
 
dc.identifier.spage5698
 
dc.identifier.urihttp://hdl.handle.net/10722/166833
 
dc.identifier.volume53
 
dc.languageeng
 
dc.publisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofInvestigative Ophthalmology & Visual Science
 
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 retinopathy
 
dc.typeArticle
 
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