December 26, 2007
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Inhibition of calpains protects against retinal ganglion cell death, study suggests

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The activation of calpains is vital for retinal ganglion cell apoptosis after calcium influx, serum starvation and optic nerve injury, according to a study by researchers in Ireland.

Thomas G. Cotter, DPhil, and colleagues at University College in Cork, Ireland, evaluated the impact of calpains on retinal ganglion cell (RGC) apoptosis and the protection calpain inhibitors can provide against cell death. The study involved two separate models of RGC apoptosis, including the RGC-5 cell line after either intracellular calcium influx or serum starvation, and retinal explant culture involving optic nerve axotomy, according to the study.

In the RGC-5 cell line, the researchers noted the activation of µ-calpain and m-calpain after serum starvation and calcium ionophore treatment, "with concurrent cleavage of known calpain substrates," the authors reported.

Protein analysis of the retinal explant culture demonstrated calpain activation after axotomy, "with concomitant cleavage of calpain substrates," they wrote.

"[Inhibition] of calpains significantly protected cells in the GCL from cell death," they said.

The study is published in the December issue of Investigative Ophthalmology & Visual Science.