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Editors Selection IGR 13-3
Basic Research - RGC: Activation of autophagy
Comment by Natik Piri on:
47112 Activation of autophagy in a rat model of retinal ischemia following high intraocular pressure, Piras A; Gianetto D; Conte D et al., PLoS ONE, 2011; 6: 22514
The association of autophagic cell death with neuronal degeneration in a high intraocular pressure (IOP) induced rat model of ischemia was evaluated by Piras et al. (1246). The presence of LAMP1 (a lysosomal marker) positive cytoplasmic granules in the ganglion cell layer and inner nuclear layer, and an increase in the level of LC3-II (autophagy marker), indicate an activation of autophagic process in the retina following ischemia/reperfusion (I/R) injury. The expression of these lysosome/autophagosome-associated markers was observed 12 h (LAMP1) and 24 h (LAMP1 and LC3-II) and was undetectable 48 h after insult. Pharmacological inhibition of autophagy with 3-methyladenine reduced the level of GFAP immunoreactivity associated with the activation of Müller cells and led to an increase in neuronal survival. Since autophagy is known to be involved in both cell protection and cell death, the results of this study indicate that the activation of autophagy in response to I/R injury is associated with autophagic neuronal death. These experiments were performed 24 h after injury and in order to evaluate the long-term effect of autophagy inhibition on reactive astrogliosis and ganglion cell protection from retinal ischemia, further studies are needed. The data presented in this paper complement earlier observations on autophagy activation in animal models of RGC degeneration, such as optic nerve transection (Kim et al., 2008; Rodríguez-Muela et al., 2011), optic nerve crush (Knoferle et al., 2010), as well as in the high IOP-induced retinal ischemia model (Russo et al., 2011).
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