Sodium Iodate Disrupted the Mitochondrial-Lysosomal Axis in Cultured Retinal Pigment Epithelial Cells
Abstract
Low doses of sodium iodate (NaIO3) impair visual function in experimental animals with selective damage to retinal pigment epithelium (RPE) and serve as a useful model to study diseases caused by RPE degeneration. Mitochondrial dysfunction and defective autophagy have been suggested to play important roles in normal aging as well as many neurodegenerative diseases. In this study, we examined whether NaIO3 treatment disrupted the mitochondrial-lysosomal axis in cultured RPE. The human RPE cell line, ARPE-19, was treated with low concentrations (≤500 μM) of NaIO3. The expression of proteins involved in the autophagic pathway and mitochondrial biogenesis was examined with Western blot. Intracellular acidic compartments and lipofuscinogenesis were evaluated by acridine orange staining and autofluorescence, respectively. Mitochondrial mass, mitochondrial membrane potential (MMP), and mitochondrial function were quantified by MitoTracker Green staining, tetramethylrhodamine methyl ester staining, and the MTT assay, respectively. Phagocytosis and the degradation of photoreceptor outer segments (POS) were assessed by fluorescence-based approaches and Western blot against rhodopsin. Treatment with low concentrations of NaIO3 decreased c...Continue Reading
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