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This research aimed to dissect the function of TYRP1 and PMEL in glaucomatous animal and cell models. A chronic ocular hypertension (COH) rat model was induced in the right eyes of rats through the electrocoagulation of superficial iris veins. In addition, an oxygen–glucose deprivation (OGD)-retinal ganglion cell (RGC) model was constructed through OGD. TYRP1 and PMEL expression was altered in the animal and cell models to explore their effects. TYRP1 and PMEL expression was poor in glaucoma patients, COH rats, and OGD-RGCs. Mechanistically, TYRP1 interacted with PMEL to upregulate PMEL in OGD-RGCs. TYRP1 overexpression enhanced viability and diminished apoptosis and oxidative stress of OGD-RGCs, which was abolished by PMEL knockdown. TYRP1 upregulation reduced intraocular pressure, RGC apoptosis, and oxidative stress in COH rats, which was reversed by PMEL knockdown. TYRP1 elevates PMEL expression to reduce RGC apoptosis and oxidative stress in vivo and in vitro.

TYRP1 Protects Against the Apoptosis and Oxidative Stress of Retinal Ganglion Cells by Binding to PMEL