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Mitochondrial replacement in an iPSC model of Leber’s hereditary optic neuropathy.

Mitochondrial replacement in an iPSC model of Leber’s hereditary optic neuropathy.
Author Information (click to view)

Wong RCB, Lim SY, Hung SSC, Jackson S, Khan S, Van Bergen NJ, De Smit E, Liang HH, Kearns LS, Clarke L, Mackey DA, Hewitt AW, Trounce IA, Pébay A,


Wong RCB, Lim SY, Hung SSC, Jackson S, Khan S, Van Bergen NJ, De Smit E, Liang HH, Kearns LS, Clarke L, Mackey DA, Hewitt AW, Trounce IA, Pébay A, (click to view)

Wong RCB, Lim SY, Hung SSC, Jackson S, Khan S, Van Bergen NJ, De Smit E, Liang HH, Kearns LS, Clarke L, Mackey DA, Hewitt AW, Trounce IA, Pébay A,

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Aging 2017 04 29() doi 10.18632/aging.101231
Abstract

Cybrid technology was used to replace Leber hereditary optic neuropathy (LHON) causing mitochondrial DNA (mtDNA) mutations from patient-specific fibroblasts with wildtype mtDNA, and mutation-free induced pluripotent stem cells (iPSCs) were generated subsequently. Retinal ganglion cell (RGC) differentiation demonstrates increased cell death in LHON-RGCs and can be rescued in cybrid corrected RGCs.

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