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Editors Selection IGR 11-1

Basic Research: Latanoprost as neuroprotective agent

Comment by Neville Osborne on:

The experimental data reported by Kanamori et al. (340) show that latanoprost acid acts as a neuroprotective agent. Three other reports exist, where the same conclusion was reached. The implication from all four studies is that latanoprost acid used routinely to lower elevated intraocular pressure in glaucoma patients will also directly have a beneficial effect on ganglion cell survival if it reaches the retina. It remains unclear however, how latanoprost acid is able to blunt the variety of insults to retinal cells in situ and in vitro. Latanoprost acid attenuates ganglion cell death in situ induced experimentally either by optic nerve crush (Kanamura et al. 2009), NMDA administration (Kuda et al. 2006), ischemia (Drago et al. 2001) or diabetes (Nakanishi et al. 2006). Moreover, latanoprost acid increases the survival of primary retinal cell cultures and retinal cell lines (RGC-5 and R28 cells) where insults are by serum deprivation or excessive glutamate. In the case of serum deprivation, the latanoprost acid effect is blunted by UO126, a mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (MEK) 1 and 2 inhibitor (Kanamura et al. 2009, Nakanishi et al. 2006). All these studies clearly provide a strong case for latanoprost acid being a potent neuroprotective agent to damaged ganglion cells. Since latanoprost acid is known to have a high affinity for specific FP receptors their association with ganglion cells is implicated. Clearly more studies are necessary to determine whether this is the case. Additional studies may also explain why in some studies latanoprost acid is an effective neuroprotectant in vitro specifically at concentrations less than 1 µM (Drago et al. 2001) and only at greater concentrations in other reports (Kanamori et al. 2009).

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