SNJ-1945 inhibited calpain activation, but z-VAD-fmk did not. (2) Incubation under hypoxia alone induced activation of calpain, but not caspases. (1) Hypoxia and A2E each decreased viability of RPE cells in a time-dependent manner. Calpain inhibitor, SNJ-1945, and pan-caspase inhibitor, z-VAD-fmk, were used to confirm activation of the proteases. Immunoblotting was used to detect activation of calpain and caspase. Monkey primary RPE cells were cultured under hypoxic conditions in a Gaspak pouch or cultured with synthetic A2E. The purpose of the present study is to compare activation of calpain and caspase in monkey RPE cells cultured under hypoxia or with A2E. Several mechanisms have been proposed: (1) age-related failure of the choroidal vasculature leads to loss of RPE (2) RPE dysfunctions due to accumulation of phagocytized, but unreleased A2E ( N-retinylidene- N-retinylethanolamine) (3) zinc deficiency activation of calpain and caspase proteases, leading to cell death. AMD is the leading cause of human vision loss after 65 years of age.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |