Taurine protects transformed rat retinal ganglion cells from hypoxia-induced apoptosis by preventing mitochondrial dysfunction

Abstract

Hypoxia-induced apoptosis of retinal ganglion cells (RGCs) is the major cause of progressive vision loss in numerous retinal diseases, including glaucoma and diabetic retinopathy. Taurine is a naturally occurring free amino acid that has been shown to have neurotrophic and neuroprotective properties in the retina. We investigated the specific potential for taurine to be protective for immortalized rat retinal ganglion cells (RGC-5) exposed to hypoxia (5% O(2)). Pretreatment of RGC-5 cells with 0.1 mM taurine significantly reduced the extent of apoptosis detected by DAPI staining, MTT, and Annexin V-FITC/PI assays. To further study the mechanism underlying the beneficial effect of taurine, interactions between taurine and the process of mitochondria-mediated apoptosis were examined. Taurine treatment of RGC-5 cells suppressed the induction of the mitochondrial permeability transition (mPT) by reducing intracellular calcium levels and inhibiting the opening of mitochondrial permeability transition pores (mPTPs). Moreover, the loss of mitochondrial membrane potential, a decline in cellular ATP levels, a reduction in the amount of cytochrome c translocated to the cytoplasm and caspase-3 activation were observed in taurine-treated cultures. These results demonstrate the potential for taurine to protect RGCs against hypoxic damage in vivo by preventing mitochondrial dysfunction.