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Conference Paper: Aldose reductase deficiency protects the retinal neurons in a mouse model of retinopathy of prematurity

TitleAldose reductase deficiency protects the retinal neurons in a mouse model of retinopathy of prematurity
Authors
Issue Date2012
PublisherHKSN & BPHK.
Citation
The 2012 Joint Annual Scientific Meeting of Hong Kong Society of Neurosciences and the Biophysical Society of Hong Kong, Hong Kong, 14-15 June 2012. In Program Book, 2012, p. 75-76 How to Cite?
AbstractPURPOSE: Retinopathy of prematurity (ROP) is a common retinal disease occurred in premature babies. It is found to be related to oxidative stress while dysfunction of the neural retina has also been documented. We previously showed that genetic deletion or pharmacological inhibition of aldose reductase (AR), a rate- limiting enzyme in the polyol pathway, prevented ischemia-induced retinal ganglion cell (RGC) loss and oxidative stress. Here, we assessed the effects of AR deletion on retinal neurons using a mouse model of ROP. METHODS: Seven-day-old mouse pups were exposed to 75% oxygen for five days and returned to room air. The pathological neuronal changes were examined and compared between wild-type (WT) and AR-deficient retinae on P14 and P17 (P, postnatal). Retinal thickness was measured and immunohistochemistry for calbindin, calretinin, PKCα, Tuj1, glial fibrillary acidic protein (GFAP), nitrotyrosine (NT), as well as poly(ADP-ribose) (PAR) was performed. RESULTS: After hyperoxia exposure, significantly reduced inner nuclear layer (INL) and inner plexiform layer (IPL) thickness were found in both genotypes. The intensity of calbindin staining for horizontal cells in INL was reduced in the WT retinae but not in AR-deficient retinae. In addition, significant reduction was found in calretinin-positive amacrine cell bodies in central INL especially in WT retinae. Serious distortion was also observed in the three calretinin-positive strata along IPL in the WT retinae but not AR-deficient retinae on P17. Moreover, increased GFAP intensity across IPL indicating Müller cell processes was observed in AR-deficient retinae on P14 and in WT retinae on P17. Furthermore, increased NT immunoreactivity in INL and nuclear or para-nuclear PAR staining along GCL were observed in WT retina while these changes were not apparent in AR-deficient retina. CONCLUSION: Our observations demonstrated morphological changes of retinal neurons in the mouse model of ROP and indicated that AR deficiency showed neuronal protection in the retina, possibly through modulating glial responses and reducing oxidative stress.
DescriptionPoster Presentation: P64
Persistent Identifierhttp://hdl.handle.net/10722/160135

 

DC FieldValueLanguage
dc.contributor.authorFu, Zen_US
dc.contributor.authorLi, SYen_US
dc.contributor.authorWong, Den_US
dc.contributor.authorChung, SKen_US
dc.contributor.authorLo, ACYen_US
dc.date.accessioned2012-08-16T06:04:09Z-
dc.date.available2012-08-16T06:04:09Z-
dc.date.issued2012en_US
dc.identifier.citationThe 2012 Joint Annual Scientific Meeting of Hong Kong Society of Neurosciences and the Biophysical Society of Hong Kong, Hong Kong, 14-15 June 2012. In Program Book, 2012, p. 75-76en_US
dc.identifier.urihttp://hdl.handle.net/10722/160135-
dc.descriptionPoster Presentation: P64-
dc.description.abstractPURPOSE: Retinopathy of prematurity (ROP) is a common retinal disease occurred in premature babies. It is found to be related to oxidative stress while dysfunction of the neural retina has also been documented. We previously showed that genetic deletion or pharmacological inhibition of aldose reductase (AR), a rate- limiting enzyme in the polyol pathway, prevented ischemia-induced retinal ganglion cell (RGC) loss and oxidative stress. Here, we assessed the effects of AR deletion on retinal neurons using a mouse model of ROP. METHODS: Seven-day-old mouse pups were exposed to 75% oxygen for five days and returned to room air. The pathological neuronal changes were examined and compared between wild-type (WT) and AR-deficient retinae on P14 and P17 (P, postnatal). Retinal thickness was measured and immunohistochemistry for calbindin, calretinin, PKCα, Tuj1, glial fibrillary acidic protein (GFAP), nitrotyrosine (NT), as well as poly(ADP-ribose) (PAR) was performed. RESULTS: After hyperoxia exposure, significantly reduced inner nuclear layer (INL) and inner plexiform layer (IPL) thickness were found in both genotypes. The intensity of calbindin staining for horizontal cells in INL was reduced in the WT retinae but not in AR-deficient retinae. In addition, significant reduction was found in calretinin-positive amacrine cell bodies in central INL especially in WT retinae. Serious distortion was also observed in the three calretinin-positive strata along IPL in the WT retinae but not AR-deficient retinae on P17. Moreover, increased GFAP intensity across IPL indicating Müller cell processes was observed in AR-deficient retinae on P14 and in WT retinae on P17. Furthermore, increased NT immunoreactivity in INL and nuclear or para-nuclear PAR staining along GCL were observed in WT retina while these changes were not apparent in AR-deficient retina. CONCLUSION: Our observations demonstrated morphological changes of retinal neurons in the mouse model of ROP and indicated that AR deficiency showed neuronal protection in the retina, possibly through modulating glial responses and reducing oxidative stress.-
dc.languageengen_US
dc.publisherHKSN & BPHK.-
dc.relation.ispartofJoint Annual Scientific Meeting of Hong Kong Society of Neurosciences & the Hong Kong Biophysical Societyen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleAldose reductase deficiency protects the retinal neurons in a mouse model of retinopathy of prematurityen_US
dc.typeConference_Paperen_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@hkucc.hku.hken_US
dc.identifier.authorityWong, D=rp00516en_US
dc.identifier.authorityChung, SK=rp00381en_US
dc.identifier.authorityLo, ACY=rp00425en_US
dc.description.naturepostprint-
dc.identifier.hkuros205741en_US
dc.identifier.spage75-
dc.identifier.epage76-
dc.publisher.placeHong Kong-

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