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month download article/chapter aspartate receptor–mediated neurotoxicity human cystine/glutamate transporter streptozotocin–induced diabetic mice allen jw dl–alpha–aminoadipate toxicity intracellular gsh level cystine/glutamate antiporter expression primary culture glutamate–cystine antiporter xct retinal ganglion cells cystine-glutamate exchanger retinal muller cells radial glial cells rgc–5 cell line full article pdf caspase–mediated apoptosis cystine–glutamate exchange oxidative stress upregulates related subjects neuronal oxidative stress article cell neonatal mouse retinas mouse peritoneal macrophages cultured primary astrocytes retinal cells exposed privacy choices/manage cookies rat brain slices diabetes–induced dysfunction tissue research aims retinal pigment epithelium cystine–glutamate antiporter reactive oxygen species amino acid exchangers interleukin–10 receptor signaling cultured retinal neurons abnormal retinal electrophysiology blood–retinal barrier nitric oxide donor check access instant access glial cells gardner tw health grants ey014560 early retinal complications extracellular glutamate concentration barber aj fetal brain cells na+-independent exchange xct gene expression

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         headline:Expression of the cystine-glutamate exchanger (xc −) in retinal ganglion cells and regulation by nitric oxide and oxidative stress
         description:The cystine-glutamate exchanger, system xc −, mediates the Na+-independent exchange of cystine into cells, coupled to the efflux of intracellular glutamate. System xc − plays a critical role in glutathione homeostasis. Early studies of brain suggested that system xc − was present primarily in astrocytes but not neurons. More recent work indicates that certain brain neurons have an active system xc −. In the retina, system xc − has been demonstrated in Müller and retinal pigment epithelial cells. We have recently suggested that two protein components of system xc −, xCT and 4F2hc, are present in ganglion cells of the intact retina. Here, we have used (1) molecular and immunohistochemical assays to determine whether system xc − is present in primary ganglion cells isolated from neonatal mouse retinas and (2) functional assays to determine whether its activity is regulated by oxidative stress in a retinal ganglion cell line (RGC–5). Primary mouse ganglion cells and RGC–5 cells express xCT and 4F2hc. RGC–5 cells take up [3H]glutamate in the absence of Na+, and this uptake is blocked by known substrates of system xc − (glutamate, cysteine, cystine, quisqualic acid). Treatment of RGC–5 cells with NO and reactive oxygen species donors leads to increased activity of system xc − associated with an increase in the maximal velocity of the transporter with no significant change in the substrate affinity. This is the first report of system xc − in primary retinal ganglion cells and RGC–5 cells. Oxidative stress upregulates this transport system in RGC–5 cells, and the process is associated with an increase in xCT mRNA and protein but no change in 4F2hc mRNA or protein.
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      description:The cystine-glutamate exchanger, system xc −, mediates the Na+-independent exchange of cystine into cells, coupled to the efflux of intracellular glutamate. System xc − plays a critical role in glutathione homeostasis. Early studies of brain suggested that system xc − was present primarily in astrocytes but not neurons. More recent work indicates that certain brain neurons have an active system xc −. In the retina, system xc − has been demonstrated in Müller and retinal pigment epithelial cells. We have recently suggested that two protein components of system xc −, xCT and 4F2hc, are present in ganglion cells of the intact retina. Here, we have used (1) molecular and immunohistochemical assays to determine whether system xc − is present in primary ganglion cells isolated from neonatal mouse retinas and (2) functional assays to determine whether its activity is regulated by oxidative stress in a retinal ganglion cell line (RGC–5). Primary mouse ganglion cells and RGC–5 cells express xCT and 4F2hc. RGC–5 cells take up [3H]glutamate in the absence of Na+, and this uptake is blocked by known substrates of system xc − (glutamate, cysteine, cystine, quisqualic acid). Treatment of RGC–5 cells with NO and reactive oxygen species donors leads to increased activity of system xc − associated with an increase in the maximal velocity of the transporter with no significant change in the substrate affinity. This is the first report of system xc − in primary retinal ganglion cells and RGC–5 cells. Oxidative stress upregulates this transport system in RGC–5 cells, and the process is associated with an increase in xCT mRNA and protein but no change in 4F2hc mRNA or protein.
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         Molecular Medicine
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