Protective Effects of Mitochondria-Targeted Peptide MTP-131 on Trabecular Meshwork Cells under Elevated Hydrostatic Pressure

To investigate the effects of MTP-131 on trabeculum cells cultured under hydrostatic pressure Glaucomatous human trabecular meshwork (GTM3) cells were divided into three groups: the MTP-131 group, the hydrostatic group, and the normal group. The MTP-131 group was pretreated with 1 µM MTP-131, and the cells were then cultured under 80 mmHg pressure for 24 hours. The normal group was cultured under normal atmospheric pressure for 24 h, and the hydrostatic group was cultured under 80 mmHg pressure for 24 h. The change in the mitochondrial membrane potential the generation of reactive oxygen species (ROS) and the release of cytochrome c from the mitochondria were analyzed with confocal microscopy. The generation of ROS and apoptosis were detected by flow cytometry. The expression of caspase-3 was detected by western blot analysis. In GTM3 cells, culturing under hydrostatic pressure resulted in a decrease in the mitochondrial membrane potential, an elevation of intracellular ROS and a release of cytochrome c from the mitochondria. Pretreatment with MTP-131 prevented the mitochondrial depolarization, decreased the intracellular ROS, prohibited the release of cytochrome c from the mitochondria and inhibited apoptosis. The path of apoptosis is caspase-3 independent. MTP-131 can protect cultured trabecular cells from the damage caused by hydrostatic pressure.