Induction of BIMEL following growth factor withdrawal is a key event in caspase-dependent apoptosis of 661W photoreceptor cells

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Apoptosis of photoreceptor cells in the early postnatal period is a normal feature of mammalian retinal development. The role of mitochondria and caspases in the process has been well established; however, the identification of key apoptotic mediators still remains elusive. Here we report that BIMEL, a pro-apoptotic BCL-2 family member, may be one such molecule. Following growth factor deprivation, BIMEL was up-regulated in mouse 661W cone photoreceptors. This event correlated with the release of mitochondrial apoptogenic factors into the cytosol, the activation of caspases and apoptosis. Moreover, a similar behaviour was observed in response to UV radiation, ionomycin or H2O2 treatments. We identified the PI3K–Akt–FKHRL1 signalling cascade as the main regulatory pathway of BIMEL expression in these cells. Finally, using RNA interference, we were able to silence BIMEL expression and subsequently suppress caspase-3 activation. In conclusion, we propose BIMEL as a critical factor in mitochondria-dependent apoptosis of 661W photoreceptors.

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