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Editors Selection IGR 13-2

Neuroprotection: Calcineurin

Comment by Manuel Vidal-Sanz on:

13328 Calcineurin cleavage is triggered by elevated intraocular pressure, and calcineurin inhibition blocks retinal ganglion cell death in experimental glaucoma, Huang W; Fileta JB; Dobberfuhl A et al., Proceedings of the National Academy of Sciences of the United States of America, 2005; 102: 12242-12247

See also comment(s) by Leonard A. Levin •

Find related abstracts

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Rodent models with elevated intraocular pressure (IOP), whether spontaneous (e.g., the DBA/2J mice) or induced, are useful paradigms to study the mechanisms involved in retinal ganglion cell (RGC) death as well as its possible prevention (neuroprotection). Huang et al. (41) have examined the role of calcineurin (CaN) cleavage in rodents with elevated IOP-induced RGC loss and suggest that blockage of CaN may be a neuroprotective approach to prevent RGC loss in glaucoma.

The authors found CaN cleavage to be associated with elevated IOP. Indeed, elevated cleaved CaN was found in rats with

Calcineurin inhibition may be an interesting approach to protect RGC death in glaucoma

hypertonic saline induced-elevation of the IOP and in DBA/2J mice with elevated IOP, but not in DBA/2J mice with normal IOP or in rats with complete intraorbital optic nerve crush. Further evidence in favor of CaN cleavage involvement in RGC death was obtained from a group of animals in which oral treatment with the CaN inhibitor FK506 resulted in significant protection against IOP-induced RGC loss. The neuroprotective effect of FK506 was documented in a stereological analysis of the RGC population (identified with neuronal tracers injected into the superior colliculi one week prior to IOP-induction) and in a morphological analysis of the optic nerves in cross sections. Overall this line of work suggests that CaN inhibition may be an interesting approach to protect RGC death in glaucoma

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