Mitochondrial Protection by Exogenous Otx2 in Mouse Retinal Neurons | Zendy

Hyoung-Tai Kim | Zendy; Soung Jung Kim | Zendy; Young-In Sohn | Zendy; Sun-Sook Paik | Zendy; Romain Caplette | Zendy; Manuel Simonutti | Zendy; Kyeong Hwan Moon | Zendy; Eun Jung Lee | Zendy; Kwang Wook Min | Zendy; Mi Jeong Kim | Zendy; DongGi Lee | Zendy; Antonio Simeone | Zendy; Thomas Lamonerie | Zendy; Takahisa Furukawa | Zendy; Jong-Soon Choi | Zendy; Hee-Seok Kweon | Zendy; Serge Picaud | Zendy; InBeom Kim | Zendy; Minho Shong | Zendy; Jin Woo Kim | Zendy

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Mitochondrial Protection by Exogenous Otx2 in Mouse Retinal Neurons

Author(s) -

Hyoung-Tai Kim,

Soung Jung Kim,

Young-In Sohn,

Sun-Sook Paik,

Romain Caplette,

Manuel Simonutti,

Kyeong Hwan Moon,

Eun Jung Lee,

Kwang Wook Min,

Mi Jeong Kim,

DongGi Lee,

Antonio Simeone,

Thomas Lamonerie,

Takahisa Furukawa,

Jong-Soon Choi,

Hee-Seok Kweon,

Serge Picaud,

InBeom Kim,

Minho Shong,

Jin Woo Kim

Publication year - 2015

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2015.09.075

Subject(s) - retinal , microbiology and biotechnology , mitochondrion , biology , neuroprotection , retina , mitochondrial fusion , dystrophy , mitochondrial dna , neuroscience , genetics , gene , biochemistry

OTX2 (orthodenticle homeobox 2) haplodeficiency causes diverse defects in mammalian visual systems ranging from retinal dysfunction to anophthalmia. We find that the retinal dystrophy of Otx2(+/GFP) heterozygous knockin mice is mainly due to the loss of bipolar cells and consequent deficits in retinal activity. Among bipolar cell types, OFF-cone bipolar subsets, which lack autonomous Otx2 gene expression but receive Otx2 proteins from photoreceptors, degenerate most rapidly in Otx2(+/GFP) mouse retinas, suggesting a neuroprotective effect of the imported Otx2 protein. In support of this hypothesis, retinal dystrophy in Otx2(+/GFP) mice is prevented by intraocular injection of Otx2 protein, which localizes to the mitochondria of bipolar cells and facilitates ATP synthesis as a part of mitochondrial ATP synthase complex. Taken together, our findings demonstrate a mitochondrial function for Otx2 and suggest a potential therapeutic application of OTX2 protein delivery in human retinal dystrophy.

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