Mitochondrial ROS in Slc4a11 KO Corneal Endothelial Cells Lead to ER Stress.

ABSTRACT: Recent studies from Slc4a11 ^-/- mice have identified glutamine-induced mitochondrial dysfunction as a significant contributor toward oxidative stress, impaired lysosomal function, aberrant autophagy, and cell death in this Congenital Hereditary Endothelial Dystrophy (CHED) model. Because lysosomes are derived from endoplasmic reticulum (ER)-Golgi, we asked whether ER function is affected by mitochondrial ROS in Slc4a11 KO corneal endothelial cells. In mouse Slc4a11 ^-/- corneal endothelial tissue, we observed the presence of dilated ER and elevated expression of ER stress markers BIP and CHOP. Slc4a11 KO mouse corneal endothelial cells incubated with glutamine showed increased aggresome formation, BIP and GADD153, as well as re

SUBMITTER: Shyam R 

PROVIDER: S-EPMC9086159 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature