Connexin hemichannels regulate redox potential via metabolite exchange and protect lens against cellular oxidative damage.
Ontology highlight
ABSTRACT: Increased oxidative stress contributes to cataract formation during aging. Anterior epithelial cells are a frontline antioxidant defense system with powerful capacities to maintain redox homeostasis and lens transparency. In this study, we report a new molecular mechanism of connexin (Cx) hemichannels (HCs) in lens epithelial cells to protect lens against oxidative stress. Our results showed haploinsufficiency of Cx43 elevated oxidative stress and susceptibility to cataracts in the mouse lens. Cx43 HCs opened in response to hydrogen peroxide (H2O2) or ultraviolet radiation (UVR) in human lens epithelium HLE-B3 cells, and this activation contributed to a cellular protective mechanism against oxidative stress-induced apoptotic cell death. Furthermore, we found that Cx43
SUBMITTER: Quan Y
PROVIDER: S-EPMC8408634 | biostudies-literature | 2021 Oct
REPOSITORIES: biostudies-literature
ACCESS DATA