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

Abstract

OBJECTIVES: This research aimed to dissect the function of TYRP1 and PMEL in glaucomatous animal and cell models. METHODS: 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. RESULTS: 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. CONCLUSIONS: TYRP1 elevates PMEL expression to reduce RGC apoptosis and oxidative stress in vivo and in vitro.