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Conference Paper: Aldose Reductase Deficiency Protects the Neonatal Mouse Retina Against Oxygen-Induced Retinopathy

TitleAldose Reductase Deficiency Protects the Neonatal Mouse Retina Against Oxygen-Induced Retinopathy
Authors
Issue Date2014
PublisherInternational Society for Eye Research (ISER).
Citation
The XXI Biennial Meeting of the International Society for Eye Research (ISER), San Francisco, California, USA, 20-24 July 2014. In the Program and Abstract Book of the XXI Biennial Meeting of the International Society for Eye Research (ISER), 2014, p. 254, abstract no 218 How to Cite?
AbstractRetinopathy of prematurity (ROP) has become the leading cause of blindness and visual loss in children. Besides the wellknown vascular abnormality, retinal dysfunction has also been reported even after ROP has resolved. We previously showed that genetic deletion of aldose reductase (AR), the rate-limiting enzyme in the polyol pathway, protected the neonatal vasculature and reduced neovascularization in the mouse model of oxygen-induced retinopathy (OIR), a well-established model of ROP. Here, we further investigated the effects of AR deficiency on retinal neuronal function and morphology. Seven- day-old wild-type (WT) and AR-deficient (AR-/-) mouse pups were exposed to 75% oxygen for 5 days and then returned to room air. Electroretinography was used to examine the retinal function at P30. Retinal layer thickness was measured and compared. Various retinal neurons were identified by immunohistochemistry for calbindin (horizontal cell marker), PKCα (rod bipolar cell marker), calretinin (amacrine cell marker), and Tuj1 (retinal ganglion cell marker). Level of oxidative stress was assessed by immunohistochemistry for poly(ADP-ribose) (PAR). Our results showed that significantly reduced a-wave, b-wave and OPs were observed in WT but not in AR-/- mice. While there was significantly reduced retinal inner nuclear layer and inner plexiform layer thickness in WT central retinae, AR-/- retinae showed preserved inner nuclear layer and inner plexiform layer. Horizontal, rod bipolar and amacrine cells were partly protected by AR deficiency with an attenuated PAR immunoreactivity. Our results not only demonstrated the retinal neuronal changes in the mouse model of OIR, but also showed that these changes appeared to be prominent in central avascular area, indicating a link between vascular abnormality and neuronal changes. In addition, AR deficiency provides protection in retinal neurons possibly by reducing oxidative stress, suggesting a therapeutic potential of AR inhibition in the treatment of ROP with beneficial effects on retinal neurons.
DescriptionPoster session 2
Persistent Identifierhttp://hdl.handle.net/10722/199844

 

DC FieldValueLanguage
dc.contributor.authorLo, ACYen_US
dc.contributor.authorFu, Zen_US
dc.contributor.authorNian, Sen_US
dc.contributor.authorChung, SKen_US
dc.date.accessioned2014-07-22T01:41:35Z-
dc.date.available2014-07-22T01:41:35Z-
dc.date.issued2014en_US
dc.identifier.citationThe XXI Biennial Meeting of the International Society for Eye Research (ISER), San Francisco, California, USA, 20-24 July 2014. In the Program and Abstract Book of the XXI Biennial Meeting of the International Society for Eye Research (ISER), 2014, p. 254, abstract no 218en_US
dc.identifier.urihttp://hdl.handle.net/10722/199844-
dc.descriptionPoster session 2en_US
dc.description.abstractRetinopathy of prematurity (ROP) has become the leading cause of blindness and visual loss in children. Besides the wellknown vascular abnormality, retinal dysfunction has also been reported even after ROP has resolved. We previously showed that genetic deletion of aldose reductase (AR), the rate-limiting enzyme in the polyol pathway, protected the neonatal vasculature and reduced neovascularization in the mouse model of oxygen-induced retinopathy (OIR), a well-established model of ROP. Here, we further investigated the effects of AR deficiency on retinal neuronal function and morphology. Seven- day-old wild-type (WT) and AR-deficient (AR-/-) mouse pups were exposed to 75% oxygen for 5 days and then returned to room air. Electroretinography was used to examine the retinal function at P30. Retinal layer thickness was measured and compared. Various retinal neurons were identified by immunohistochemistry for calbindin (horizontal cell marker), PKCα (rod bipolar cell marker), calretinin (amacrine cell marker), and Tuj1 (retinal ganglion cell marker). Level of oxidative stress was assessed by immunohistochemistry for poly(ADP-ribose) (PAR). Our results showed that significantly reduced a-wave, b-wave and OPs were observed in WT but not in AR-/- mice. While there was significantly reduced retinal inner nuclear layer and inner plexiform layer thickness in WT central retinae, AR-/- retinae showed preserved inner nuclear layer and inner plexiform layer. Horizontal, rod bipolar and amacrine cells were partly protected by AR deficiency with an attenuated PAR immunoreactivity. Our results not only demonstrated the retinal neuronal changes in the mouse model of OIR, but also showed that these changes appeared to be prominent in central avascular area, indicating a link between vascular abnormality and neuronal changes. In addition, AR deficiency provides protection in retinal neurons possibly by reducing oxidative stress, suggesting a therapeutic potential of AR inhibition in the treatment of ROP with beneficial effects on retinal neurons.en_US
dc.languageengen_US
dc.publisherInternational Society for Eye Research (ISER).en_US
dc.relation.ispartofBiennial Meeting of the International Society for Eye Researchen_US
dc.titleAldose Reductase Deficiency Protects the Neonatal Mouse Retina Against Oxygen-Induced Retinopathyen_US
dc.typeConference_Paperen_US
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_US
dc.identifier.emailFu, Z: kirafu@hku.hken_US
dc.identifier.emailNian, S: jessnian@hku.hken_US
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_US
dc.identifier.authorityLo, ACY=rp00425en_US
dc.identifier.authorityChung, SK=rp00381en_US
dc.identifier.hkuros230943en_US
dc.identifier.spage254, abstract no 218en_US
dc.identifier.epage254, abstract no 218en_US
dc.publisher.placeUnited Statesen_US

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