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Age-related macular degeneration (AMD) mitochondria modulate epigenetic mechanisms in retinal pigment epithelial cells

Mitochondrial damage and epigenetic modifications have been implicated in the pathogenesis of Age-related Macular Degeneration (AMD). Understanding the epigenetic mechanisms driven by AMD mitochondria may help in identifying molecular targets for therapeutic intervention in AMD. We herein characterized the interplay of AMD/normal mitochondria and epigenetic regulation in human transmitochondrial retinal pigment epithelial cybrid cells (RPE) in vitro. These human RPE cybrid cell lines were created by fusing mitochondria-deficient (Rho0) ARPE-19 cells with platelets obtained from either AMD patients (AMD cybrids) or normal subjects (normal cybrids). Therefore, all cybrids had identical nuclei (derived from ARPE-19 cells) but different mitochondria derived either from AMD patients or normal subjects. Our results revealed that AMD mitochondria regulate epigenetic mechanisms i.e., methylation and acetylation status. Demethylation using 5-Aza-2'-deoxycytidine (DAC) caused differential expression of VEGF-A gene in AMD cells. Trichostatin A (TSA), an HDAC inhibitor, also influenced protein levels of VEGF-A, HIF1α, NFκB, and CFH in AMD cells. This study might advance the field of AMD research since in addition to highlighting the critical role of nuclear-mitochondrial interactions that influence epigenetic mechanisms in AMD patients, this work suggests epigenetic profiles as potential therapeutic targets for AMD.

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S1045 TSA (Trichostatin A) TSA (Trichostatin A) is an HDAC inhibitor with IC50 of ~1.8 nM in cell-free assays.

Related Targets

HDAC