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Conference Paper: Aldose reductase deficiency protects retinal neurons against oxygen-induced retinopathy

TitleAldose reductase deficiency protects retinal neurons against oxygen-induced retinopathy
Authors
KeywordsOxidative Stress
Retina
Neovascularization
Issue Date2013
PublisherSociety for Neuroscience.
Citation
The 43rd Annual Meeting of the Society for Neuroscience (SfN), San Diego, California, USA, 9-13 November 2013 How to Cite?
AbstractPURPOSE: Retinopathy of prematurity (ROP) has become the leading cause of blindness and visual loss in children. Besides the well-known vascular abnormality, retinal dysfunction has also been reported even after ROP has resolved. We previously showed that deficiency of aldose reductase (AR), the rate-limiting enzyme in the polyol pathway, protected neonatal vasculature. Here, we further investigated the effects of AR deficiency on various retinal neurons using the mouse model of oxygen-induced retinopathy (OIR), a well-established model of ROP. METHOD: Seven-day-old mouse pups were exposed to 75% oxygen for 5 days and then returned to room air. Vascular obliteration was analyzed on isolectin-stained retinal flat-mounts. Immunohistochemistry for calbindin (horizontal cell marker), PKCα (rod bipolar cell marker), calretinin (amacrine cell marker), Tuj1 (retinal ganglion cell marker), glial fibrillary acidic protein (GFAP), nitrotyrosine (NT), and poly(ADP-ribose) (PAR) was performed on retinal sections. The results were compared between wild-type (WT) and AR-deficient (AR-/-) retinae on P14 and P17 (P, postnatal). RESULTS: On P14, calbindin and calretinin immunoreactivity was decreased in WT OIR retinae while PKCα immunoreactivity was significantly increased in AR-/- OIR retinae. But no significant differences were found for Tuj1. Yet, more intense GFAP immunoreactivity in Müller cell processes was observed in AR-/- OIR retinae. Increased NT and nuclear PAR immunoreactivity were found in WT OIR retinae but not in AR-/- OIR retinae. On P17, calbindin immunoreactivity was decreased in WT OIR retinae while PKCα-positive cell bodies appeared to be less prominent in AR-/- OIR retinae. Markedly reduced calretinin immunoreactivity, seriously distorted three strata in IPL and decreased cell bodies in INL were observed in central retinal area in WT OIR retinae but not in AR-/- OIR retinae. Again, no significant differences were found in Tuj1 immunoreactivity. GFAP immunoreactivity was significantly increased in WT OIR retinae. Importantly, significantly reduced NT and nuclear PAR immunoreactivity were observed in AR-/- OIR retinae. CONCLUSION: 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 modulating glial responses and reducing oxidative stress, suggesting a therapeutic potential of AR inhibition in the treatment of ROP with beneficial effects on retinal neurons.
DescriptionPoster session 150: Sensory Disorders: Visual and Auditory
Program#150.04 & Poster#S16
Fulltext of the abstract in: http://www.abstractsonline.com/plan/ViewAbstract.aspx?cKey=f030d709-87bc-459a-9447-177daa8f4a5f&mID=3236&mKey=8d2a5bec-4825-4cd6-9439-b42bb151d1cf&sKey=7cca261a-0bb1-4dfc-be94-1f925efbd724
Persistent Identifierhttp://hdl.handle.net/10722/199836

 

DC FieldValueLanguage
dc.contributor.authorLo, ACYen_US
dc.contributor.authorFu, Zen_US
dc.contributor.authorChung, SKen_US
dc.date.accessioned2014-07-22T01:41:33Z-
dc.date.available2014-07-22T01:41:33Z-
dc.date.issued2013en_US
dc.identifier.citationThe 43rd Annual Meeting of the Society for Neuroscience (SfN), San Diego, California, USA, 9-13 November 2013en_US
dc.identifier.urihttp://hdl.handle.net/10722/199836-
dc.descriptionPoster session 150: Sensory Disorders: Visual and Auditory-
dc.descriptionProgram#150.04 & Poster#S16-
dc.descriptionFulltext of the abstract in: http://www.abstractsonline.com/plan/ViewAbstract.aspx?cKey=f030d709-87bc-459a-9447-177daa8f4a5f&mID=3236&mKey=8d2a5bec-4825-4cd6-9439-b42bb151d1cf&sKey=7cca261a-0bb1-4dfc-be94-1f925efbd724-
dc.description.abstractPURPOSE: Retinopathy of prematurity (ROP) has become the leading cause of blindness and visual loss in children. Besides the well-known vascular abnormality, retinal dysfunction has also been reported even after ROP has resolved. We previously showed that deficiency of aldose reductase (AR), the rate-limiting enzyme in the polyol pathway, protected neonatal vasculature. Here, we further investigated the effects of AR deficiency on various retinal neurons using the mouse model of oxygen-induced retinopathy (OIR), a well-established model of ROP. METHOD: Seven-day-old mouse pups were exposed to 75% oxygen for 5 days and then returned to room air. Vascular obliteration was analyzed on isolectin-stained retinal flat-mounts. Immunohistochemistry for calbindin (horizontal cell marker), PKCα (rod bipolar cell marker), calretinin (amacrine cell marker), Tuj1 (retinal ganglion cell marker), glial fibrillary acidic protein (GFAP), nitrotyrosine (NT), and poly(ADP-ribose) (PAR) was performed on retinal sections. The results were compared between wild-type (WT) and AR-deficient (AR-/-) retinae on P14 and P17 (P, postnatal). RESULTS: On P14, calbindin and calretinin immunoreactivity was decreased in WT OIR retinae while PKCα immunoreactivity was significantly increased in AR-/- OIR retinae. But no significant differences were found for Tuj1. Yet, more intense GFAP immunoreactivity in Müller cell processes was observed in AR-/- OIR retinae. Increased NT and nuclear PAR immunoreactivity were found in WT OIR retinae but not in AR-/- OIR retinae. On P17, calbindin immunoreactivity was decreased in WT OIR retinae while PKCα-positive cell bodies appeared to be less prominent in AR-/- OIR retinae. Markedly reduced calretinin immunoreactivity, seriously distorted three strata in IPL and decreased cell bodies in INL were observed in central retinal area in WT OIR retinae but not in AR-/- OIR retinae. Again, no significant differences were found in Tuj1 immunoreactivity. GFAP immunoreactivity was significantly increased in WT OIR retinae. Importantly, significantly reduced NT and nuclear PAR immunoreactivity were observed in AR-/- OIR retinae. CONCLUSION: 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 modulating glial responses and reducing oxidative stress, suggesting a therapeutic potential of AR inhibition in the treatment of ROP with beneficial effects on retinal neurons.-
dc.languageengen_US
dc.publisherSociety for Neuroscience.-
dc.relation.ispartofNeuroscience 2013en_US
dc.rightsNeuroscience 2013. Copyright © Society for Neuroscience.-
dc.subjectOxidative Stress-
dc.subjectRetina-
dc.subjectNeovascularization-
dc.titleAldose reductase deficiency protects retinal neurons 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.emailChung, SK: skchung@hkucc.hku.hken_US
dc.identifier.authorityLo, ACY=rp00425en_US
dc.identifier.authorityChung, SK=rp00381en_US
dc.identifier.hkuros230934en_US
dc.publisher.placeUnited States-

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