Identification, Expression, and Roles of the Cystine/Glutamate Antiporter in Ocular Tissues

Table 3

Summary of xCT function.

Function tested	In vivo or in vitro	Where	Results	Reference
Maintaining cysteine/cystine redox balance	In vivo	Plasma, aqueous humour, vitreous humour	Loss of xCT resulted in increased cystine levels by 2 folds while cysteine levels remained the same	[35, 13]
GSH synthesis	In vitro	HCEC, HLEC, rat retinal cell culture, ARPE-19, rat RPE, retinal epithelial cells, rat Müller cells, mouse fibroblasts	GSH levels decreased as a result of inhibition of xCT	[51, 16, 10, 46, 44, 15]
		Mouse RPE	Increased xCT expression results in increased GSH levels	[59]
	In vivo	Cerebrum, cerebellum, hippocampus, striatum, liver, kidney, thymus, spleen, lung, heart, and pancreas	No change in GSH levels between WT and xCT KO mice	[29, 20, 6, 13]
Control of extracellular glutamate levels	In vitro	Hippocampus	Glutamate released via xCT regulates glutamatergic synapse strength by reducing the number of postsynaptic AMPA receptors	[62]
		Retina	Glutamate release via xCT is distinct from the traditional Ca^2 +-dependent vesicular release of glutamate	[34]
	In vivo	Striatum, hippocampus	Extracellular glutamate levels decrease in the xCT KO mouse when compared to WT	[29, 6]

HCEC: human corneal epithelial cells; HLEC: human lens epithelial cell; ARPE-19: human retinal epithelial cell; RPE: retinal epithelial cell.