ParkinsonFranceV1, Main, Exploration, bibRecord, 000298

Donating Otx2 to support neighboring neuron survival

Identifieur interne : 000298 ( Main/Exploration ); précédent : 000297; suivant : 000299

Donating Otx2 to support neighboring neuron survival

Auteurs : Hyoung-Tai Kim [Corée du Sud] ; Alain Prochiantz [France] ; Jin Woo Kim [Corée du Sud]

Source :

BMB Reports [ 1976-6696 ] ; 2016.

RBID : PMC:4915118

Abstract

Mutations of orthodentricle homeobox 2 (OTX2) in human and mice often cause retinal dystrophy and nyctalopia, suggesting a role of OTX2 in mature retina, in addition to its functions in the development of the eye and retina. In support of this, the number of bipolar cells in Otx2^+/− post-natal mouse retina was found to be significantly lower than normal. Degeneration of the cells becomes greater as the mice age, leading to the loss of vision. Especially, the type-2 OFF-cone bipolar cells, which do not express Otx2 mRNA but carry Otx2 protein, are most sensitive to Otx2 haplodeficiency. Interestingly, this bipolar cell subpopulation imports Otx2 protein from photoreceptors to protect itself from glutamate excitotoxicity in the dark. Moreover, in the bipolar cells, the exogenous Otx2 relocates to the mitochondria to support mitochondrial ATP synthesis. This novel mitochondrial activity of exogenous Otx2 highlights the therapeutic potential of Otx2 protein transduction in retinal dystrophy. [BMB Reports 2016; 49(2): 69-70]

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4915118

DOI: 10.5483/BMBRep.2016.49.2.006
PubMed: 26779998
PubMed Central: 4915118

Affiliations:

Le document en format XML

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<author><name sortKey="Kim, Jin Woo" sort="Kim, Jin Woo" uniqKey="Kim J" first="Jin Woo" last="Kim">Jin Woo Kim</name>
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<front><div type="abstract" xml:lang="en"><p>Mutations of <italic>orthodentricle homeobox 2</italic>
 (<italic>OTX2</italic>
) in human and mice often cause retinal dystrophy and nyctalopia, suggesting a role of OTX2 in mature retina, in addition to its functions in the development of the eye and retina. In support of this, the number of bipolar cells in <italic>Otx2</italic>
<sup>+/−</sup>
 post-natal mouse retina was found to be significantly lower than normal. Degeneration of the cells becomes greater as the mice age, leading to the loss of vision. Especially, the type-2 OFF-cone bipolar cells, which do not express <italic>Otx2</italic>
 mRNA but carry Otx2 protein, are most sensitive to <italic>Otx2</italic>
 haplodeficiency. Interestingly, this bipolar cell subpopulation imports Otx2 protein from photoreceptors to protect itself from glutamate excitotoxicity in the dark. Moreover, in the bipolar cells, the exogenous Otx2 relocates to the mitochondria to support mitochondrial ATP synthesis. This novel mitochondrial activity of exogenous Otx2 highlights the therapeutic potential of Otx2 protein transduction in retinal dystrophy. [BMB Reports 2016; 49(2): 69-70]</p>
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La maladie de Parkinson en France (serveur d'exploration)

Donating Otx2 to support neighboring neuron survival

Donating Otx2 to support neighboring neuron survival

Source :

Abstract

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Le document en format XML

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	La maladie de Parkinson en France (serveur d'exploration)
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