bFGF-mediated redox activation of the PI3K/Akt pathway in retinal photoreceptor cells.

摘要: Abstract In many retinal diseases, it is the death of photoreceptors that leads to blindness. previous in vitro and vivo studies, basic fibroblast growth factor (bFGF) has been shown increase cell survival. More recently, reactive oxygen species (ROS) have also promote survival, contrary traditional view they are solely destructive molecules. Due this possible link, we hypothesised bFGF could stimulate production ROS, which turn stimulates protein kinase B (Akt) survival pathway. Flow cytometry was used measure fluorescence oxidised dihydrorhodamine, a ROS indicator, murine 661W photoreceptor line under several different conditions. Expression cyclooxygenase (Cox) enzymes evaluated by immunohistochemistry, response cells exogenous explanted mouse retina studied confocal microscopy. Exogenous addition resulted an lasted for 24 h. When inhibited, bFGF-induced phosphorylation Akt prevented. Through use inhibitors small interfering RNA line, source be Cox involve activation phospholipases A(2) + C. This pathway may occur retina, as showed expressed Cox1&2, respond increasing their levels. These results demonstrate can through Cox, activate