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Publication : Mitochondrial ferritin affects mitochondria by stabilizing HIF-1α in retinal pigment epithelium: implications for the pathophysiology of age-related macular degeneration.

First Author  Wang X Year  2016
Journal  Neurobiol Aging Volume  47
Pages  168-179 PubMed ID  27599360
Mgi Jnum  J:239557 Mgi Id  MGI:5829150
Doi  10.1016/j.neurobiolaging.2016.07.025 Citation  Wang X, et al. (2016) Mitochondrial ferritin affects mitochondria by stabilizing HIF-1alpha in retinal pigment epithelium: implications for the pathophysiology of age-related macular degeneration. Neurobiol Aging 47:168-179
abstractText  Mitochondrial ferritin (FtMt) is believed to play an antioxidant role via iron regulation, and FtMt gene mutation has been reported in age-related macular degeneration (AMD). However, little is known about FtMt's functions in the retina and any links to AMD. In this study, we observed age-related increase in FtMt and hypoxia-inducible factor-1alpha (HIF-1alpha) in murine retinal pigment epithelium (RPE). FtMt overexpression in ARPE-19 cells stabilized HIF-1alpha, and increased the secretion of vascular endothelial growth factor. Conversely, HIF-1alpha stabilization reduced the protein level of the mature, functional form of FtMt. FtMt-overexpressing ARPE-19 cells exhibited less oxidative phosphorylation but unchanged production of adenosine triphosphate, enhanced mitochondrial fission, and triggered mitophagy in a HIF-1alpha-dependent manner. These findings suggest that increased FtMt in RPE may be protective via triggering mitophagy but cause wet AMD by inducing neovascularization due to increased vascular endothelial growth factor secretion. However, reduced level of functional FtMt in RPE under hypoxia may allow dry AMD through susceptibility to age-related stress.
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