Erratum to “Multiple, parallel cellular suicide mechanisms participate in photoreceptor cell death” [Exp. Eye Res. 83 (2006) 380–389]

Light, lipids and photoreceptor survival: live or let die?

“…A crucial divergence point is the proteases involved in this demise. 54 Though activated caspase-3 expression has been detected in rds/rds photoreceptors 55 and caspase activity increases during photoreceptor apoptosis of rd and rds mice, 54 their degeneration is delayed but not prevented by Bcl-2 overexpression 56 or by caspase inhibitors. Apoptosis during development seems to rely on caspase activation through the mitochondrial pathway, as evidenced by the high expression of pro-apoptotic Bcl-2 family members such as Bax, Bak, Bim, Puma, and that of Apaf-1 and caspase-3 in the retina at early developmental times, 46,47 and the detection of caspase-3 activity in rat retinal photoreceptors during their early development in vitro.…”

“…While apoptosis is usually associated with caspase activation and chromatin fragmentation, rod cell death is characterized by chromatin fragmentation but the involvement of caspases appears to be age and disease dependent. 57 Calpain and cathepsin are activated during photoreceptor death in rd mice, 46,54,58,59 and calpain inhibition cannot prevent this death. 48 No apoptotic photoreceptors are observed in retinas of Bax/Bak double knockout mice 49 and their apoptosis is effectively prevented by Bcl-2 overexpression.…”

“…48 No apoptotic photoreceptors are observed in retinas of Bax/Bak double knockout mice 49 and their apoptosis is effectively prevented by Bcl-2 overexpression. 46,54,60 Light damage also leads to photoreceptor apoptosis, the onset of which depends on light exposure. 47 Caspases play an important role in retinas expressing mutant rhodopsin, 51-53 but are not solely responsible for carrying on photoreceptor apoptosis in inherited degenerations.…”

“…11,46,54,[69][70][71] An early and sustained increase in intracellular ROS accompanies photoreceptor apoptosis in vitro and scavenging of these ROS can prevent this apoptosis. Oxidative stress emerges as a shared theme, involved in promoting the onset of this death in multiple pathologies, irrespective of their origin.…”

“…Oxidative stress emerges as a shared theme, involved in promoting the onset of this death in multiple pathologies, irrespective of their origin. 72 Oxidative stress has been related to cone cell death in retinitis pigmentosa; 73 oxidative stress markers increase in animal models of retinitis pigmentosa and in light damage 54 whereas an increased expression of oxidative stress-related genes is observed during the progression of retinal neurodegeneration. 69 Rod and cone photoreceptors in retinal explants generate ROS when deprived of trophic support.…”