The disruption of the rod-derived cone viability gene leads to photoreceptor dysfunction and susceptibility to oxidative stress View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-02-05

AUTHORS

T Cronin, W Raffelsberger, I Lee-Rivera, C Jaillard, M-L Niepon, B Kinzel, E Clérin, A Petrosian, S Picaud, O Poch, J-A Sahel, T Léveillard

ABSTRACT

Rod-derived cone viability factor (RdCVF) is a thioredoxin-like protein, which has therapeutic potential for rod-cone dystrophies such as retinitis pigmentosa (RP). Cone loss in rodent models of RP is effectively reduced by RdCVF treatment. In this study, we investigate the physiological role of RdCVF in the retina by analyzing the phenotype of the mouse lacking the RdCVF gene, Nxnl1. Although the mice do not show an obvious developmental defect, an age-related reduction of both cone and rod function and a delay in the dark-adaptation of the retina are recorded by electroretinogram (ERG). This functional change is accompanied by a 17% reduction in cone density and a 20% reduction in thickness of the outer nuclear layer. The transcriptome of the retina reveals early changes in the expression of genes involved in programmed cell death, stress-response and redox-signaling, which is followed by a generalized injury response with increased microglial activation, GFAP, FGF2 and lipid peroxidation levels. Furthermore, cones of the mice lacking Nxnl1 are more sensitive to oxidative stress with a reduction of 65% in the cone flicker ERG amplitude measured under hyperoxic conditions. We show here that the RdCVF gene, in addition to therapeutic properties, has an essential role in photoreceptor maintenance and resistance to retinal oxidative stress. More... »

PAGES

1199-1210

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/cdd.2010.2

DOI

http://dx.doi.org/10.1038/cdd.2010.2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1037825694

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/20139892


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29 schema:description Rod-derived cone viability factor (RdCVF) is a thioredoxin-like protein, which has therapeutic potential for rod-cone dystrophies such as retinitis pigmentosa (RP). Cone loss in rodent models of RP is effectively reduced by RdCVF treatment. In this study, we investigate the physiological role of RdCVF in the retina by analyzing the phenotype of the mouse lacking the RdCVF gene, Nxnl1. Although the mice do not show an obvious developmental defect, an age-related reduction of both cone and rod function and a delay in the dark-adaptation of the retina are recorded by electroretinogram (ERG). This functional change is accompanied by a 17% reduction in cone density and a 20% reduction in thickness of the outer nuclear layer. The transcriptome of the retina reveals early changes in the expression of genes involved in programmed cell death, stress-response and redox-signaling, which is followed by a generalized injury response with increased microglial activation, GFAP, FGF2 and lipid peroxidation levels. Furthermore, cones of the mice lacking Nxnl1 are more sensitive to oxidative stress with a reduction of 65% in the cone flicker ERG amplitude measured under hyperoxic conditions. We show here that the RdCVF gene, in addition to therapeutic properties, has an essential role in photoreceptor maintenance and resistance to retinal oxidative stress.
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37 FGF2
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39 Nxnl1
40 RdCVF
41 RdCVF gene
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46 amplitude
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53 cone loss
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56 death
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61 disruption
62 dysfunction
63 dystrophy
64 early changes
65 electroretinogram
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67 expression
68 expression of genes
69 factors
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71 function
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73 generalized injury response
74 genes
75 hyperoxic conditions
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77 layer
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79 lipid peroxidation levels
80 loss
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82 mice
83 microglial activation
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85 nuclear layer
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87 outer nuclear layer
88 oxidative stress
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90 phenotype
91 photoreceptor dysfunction
92 photoreceptor maintenance
93 physiological role
94 pigmentosa
95 potential
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97 protein
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101 retina
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103 retinitis pigmentosa
104 rod function
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