Amino Acid Signatures in the Primate Retina

Kalloniatis, Michael; Marc, Robert E.; Murry, Ralph F.

doi:10.1523/jneurosci.16-21-06807.1996

Cited by 164 publications

(197 citation statements)

References 73 publications

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“…The radial processes of Mü ller cells were also labeled. This result is in agreement with D-Asp uptake pattern seen in other mammalian retinas (Kalloniatis et al, 1996). When retinas from GLAST Ϫ/Ϫ mice were examined, there was also strong D-Asp uptake by Mü ller cell bodies and radial processes (Fig.…”

Section: D-aspartate Uptake By Mü Ller Cellssupporting

confidence: 91%

“…The breadth of each histogram is variation in intracellular partitioning, with higher signal levels generally observed in the end feet. The modal levels of endogenous markers that comprise the definitive Mü ller cell signature of high taurine, high L-glutamine and low L-glutamate (Marc et al, 1995;Kalloniatis et al, 1996) are very similar between Mü ller cells from GLAST Ϫ/Ϫ and wild-type mice, with slightly higher levels in the former (median and mean values can be similarly compared with the same conclusions). However, in the very same sets of cells, the accumulation of D-aspartate in GLAST Ϫ/Ϫ Mü ller cells is clearly 50% that achieved in wild-type cells.…”

Section: D-aspartate Uptake By Mü Ller Cellsmentioning

confidence: 55%

“…5A). Based on their location and morphological features, many of the (Kalloniatis et al, 1996). Quantitation of [ 3 H]D-Asp transport by Mü ller cells was carried out as described under Materials and Methods.…”

Section: [ 3 H]d-aspartate Autoradiographymentioning

confidence: 99%

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Glutamate transport by retinal Müller cells in glutamate/aspartate transporter‐knockout mice

Sarthy

Pignataro

Pannicke

et al. 2004

Glia

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Glutamate transporters are involved in maintaining extracellular glutamate at a low level to ensure a high signal-to-noise ratio for glutamatergic neurotransmission and to protect neurons from excitotoxic damage. The mammalian retina is known to express the excitatory amino acid transporters, EAAT1-5; however, their specific role in glutamate homeostasis is poorly understood. To examine the role of the glial glutamate/ aspartate transporter (GLAST) in the retina, we have studied glutamate transport by Mü ller cells in GLAST Ϫ/Ϫ mice, using biochemical, electrophysiological, and immunocytochemical techniques. Glutamate uptake assays indicated that the K m value for glutamate uptake was similar in wild-type and GLAST Ϫ/Ϫ mouse retinas, but the V max was ϳ50% lower in the mutant. In Na ϩ -free medium, the V max was further reduced by 40%. In patch-clamp recordings of dissociated Mü ller cells from GLAST Ϫ/Ϫ mice, application of 0.1 mM glutamate evoked no current showing that the cells lacked functional electrogenic glutamate transporters. The result also indicated that there was no compensatory upregulation of EAATs in Mü ller cells. [ 3 H]D-Aspartate uptake autoradiography, however, showed that Na ϩ -dependent, high-affinity transporters account for most of the glutamate uptake by Mü ller cells, and that Na ϩ -independent glutamate transport is negligible. Additional experiments showed that the residual glutamate uptake in Mü ller cells in the GLAST Ϫ/Ϫ mouse retina is not due to known glutamate transporters-cystine-glutamate exchanger, ASCT-1, AGT-1, or other heteroexchangers. The present study shows that while several known glutamate transporters are expressed by mammalian Mü ller cells, new Na ϩ -dependent, high-affinity glutamate transporters remain to be identified.

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Section: D-aspartate Uptake By Mü Ller Cellssupporting

confidence: 91%

Section: D-aspartate Uptake By Mü Ller Cellsmentioning

confidence: 55%

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Glutamate transport by retinal Müller cells in glutamate/aspartate transporter‐knockout mice

Sarthy

Pignataro

Pannicke

et al. 2004

Glia

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“…This novel metabolomics technique quantitatively profiles metabolites (all the natural amino acids, glutathione, and many others) with cellular resolution by ultrathin tissue section arrays using hapten-specific antibodies. [133][134][135][136][137] Potential application of this tecnique is the ability to interrogate, cell-by-cell, metabolite profiles associated with biological processes. Hopefully, these different strategies will contribute to implement the current therapies through the characterization of the dominant pathways that shape metabolism within cell classes that make up RMS tumors.…”

Section: Discussionmentioning

confidence: 99%

Uncovering metabolism in rhabdomyosarcoma

Monti

Fanzani

2016

Cell Cycle

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Rhabdomyosarcoma (RMS) is a myogenic tumor classified as the most frequent soft tissue sarcoma affecting children and adolescents. The histopathological classification includes five different histotypes, with two most predominant referred as to embryonal and alveolar, the latter being characterized by adverse outcome. The current molecular classification identifies two major subsets, those harboring the fused Pax3-Foxo1 transcription factor generating from a recurrent specific translocation (fusion-positive RMS), and those lacking this signature but harboring mutations in the RAS/PI3K/AKT signalling axis (fusion-negative RMS). Since little attention has been devoted to RMS metabolism until now, in this review we summarize the “state of art” of metabolism and discuss how some of the molecular signatures found in this cancer, as observed in other more common tumors, can predict important metabolic challenges underlying continuous cell growth, oxidative stress resistance and metastasis, which could be the subject of future targeted therapies

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“…ONL outer nuclear layer, OPL outer plexiform layer, INL inner nuclear layer, IPL inner plexiform layer, GCL ganglion cell layer. Scale bar=20 μm using these methods is proportional to the logarithm of the concentration of antigen in the tissue [34][35][36].…”

Section: Expression Of Glast and Eaat4mentioning

confidence: 99%

Glutamate uptake in retinal glial cells during diabetes

et al. 2005

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Aims: Glutamate recycling is a major function of retinal Müller cells. The aim of this study was to evaluate the expression and function of glutamate transporters during diabetes. Methods: Sprague-Dawley rats were rendered diabetic by a single dose of streptozotocin (50 mg/kg). Following 12 weeks of diabetes, immunolocalisation and mRNA expression of the two glial cell transporters, GLAST and EAAT4 were evaluated using indirect immunofluorescence and real-time PCR. The function of glutamate transport was investigated at 1, 4 and 12 weeks following induction of diabetes by measuring the level of uptake of the non-metabolisable glutamate analogue, D-aspartate, into Müller cells. Results: There was no difference in the localisation of either GLAST or EAAT4 during diabetes. Although there was a small apparent increase in expression of both GLAST and EAAT4 in diabetic retinae compared with controls this was not statistically significant. At 1, 4 and 12 weeks following diabetes, D-aspartate immunoreactivity was significantly increased in Müller cells of diabetic rats compared to controls (p<0.001). The EC 50 was found to increase by 0.304 log units in diabetic Müller cells compared with controls, suggesting that glutamate uptake is twice as efficient. Conclusions: These data suggest that there are alterations in glutamate transport during diabetes. However, these changes are unlikely to play a significant role in glutamate-induced neuronal excitoxicity during diabetes. These results suggest that although Müller cells undergo gliosis at an early stage of diabetes, one of the most important functions for maintaining normal retinal function is preserved within the retina.

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Amino Acid Signatures in the Primate Retina

Cited by 164 publications

References 73 publications

Glutamate transport by retinal Müller cells in glutamate/aspartate transporter‐knockout mice

Glutamate transport by retinal Müller cells in glutamate/aspartate transporter‐knockout mice

Uncovering metabolism in rhabdomyosarcoma

Glutamate uptake in retinal glial cells during diabetes

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