Excitatory Amino Acid Transporter 5 is widely expressed in peripheral tissues

Lee, A.; Anderson, Ashley; Stevens, Melissa G.; Beasley, Shannon J.; Barnett, Nigel L.; Pow, David V.

doi:10.4081/ejh.2013.e11

Cited by 19 publications

(21 citation statements)

References 27 publications

(36 reference statements)

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“…EAAT5 has also been detected in cerebellum (Ochiai et al, 2010) and tissues such as the vestibular system (Dalet et al, 2012) and testis (Lee et al, 2011a). More recent studies of EAAT5 using a newly developed antibody showed abundant expression in many non-nervous tissues including liver, kidney, intestine, heart, lung and skeletal muscle (Lee et al, 2013). Collectively, these findings dispel the widely held notion that the expression of EAAT5 is confined to the retina.…”

Section: Introductionmentioning

confidence: 85%

A novel splice variant of the Excitatory Amino Acid Transporter 5: Cloning, immunolocalization and functional characterization of hEAAT5v in human retina

Lee

Stevens

Anderson

et al. 2016

Neurochemistry International

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. have performed immunocytochemistry to demonstrate expression in photoreceptors in human retina. We noted that in retinas afflicted by dry aged-related macular degeneration (AMD), there was a loss of hEAAT5v from the lesioned area and from photoreceptors adjacent to the lesion. We conclude that hEAAT5v protein expression may be perturbed in peri-lesional areas of AMD-afflicted retinas that do not otherwise exhibit evidence of damage. The loss of hEAAT5v could, therefore, represent an early pathological change in the development of AMD and might be involved in its aetiology.

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Section: Introductionmentioning

confidence: 85%

A novel splice variant of the Excitatory Amino Acid Transporter 5: Cloning, immunolocalization and functional characterization of hEAAT5v in human retina

Lee

Stevens

Anderson

et al. 2016

Neurochemistry International

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“…It is present in vestibular hair cells (Dalet et al, 2012), in the heart (Arriza et al, 1997;Martinov et al, 2014), in skeletal muscle (Arriza et al, 1997) and possibly at low levels in several other peripheral organs (Lee et al, 2013).…”

Section: Eaat4mentioning

confidence: 99%

Neuronal vs glial glutamate uptake: Resolving the conundrum

Danbolt

Furness

Zhou

2016

Neurochemistry International

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Neither normal brain function nor the pathological processes involved in neurological diseases can be adequately understood without knowledge of the release, uptake and metabolism of glutamate. The reason for this is that glutamate (a) is the most abundant amino acid in the brain, (b) is at the cross-roads between several metabolic pathways, and (c) serves as the major excitatory neurotransmitter. In fact most brain cells express glutamate receptors and are thereby influenced by extracellular glutamate. In agreement, brain cells have powerful uptake systems that constantly remove glutamate from the extracellular fluid and thereby limit receptor activation. It has been clear since the 1970s that both astrocytes and neurons express glutamate transporters. However, the relative contribution of neuronal and glial transporters to the total glutamate uptake activity, however, as well as their functional importance, has been hotly debated ever since. The present short review provides (a) an overview of what we know about neuronal glutamate uptake as well as an historical description of how we got there, and (b) a hypothesis reconciling apparently contradicting observations thereby possibly resolving the paradox. ABBREVIATIONSCre, Cyclization recombinase (Le and Sauer, 2000); EAAC1, glutamate transporter (EAAT3; slc1a1; Kanai and Hediger, 1992; Bjørås et al., 1996); EAAT, excitatory amino acid transporter (synonym to glutamate transporter); GABA, γ-aminobutyric acid; GLAST, rat glutamate transporter (EAAT1; slc1a3; Storck et al., 1992;Tanaka, 1993a); GLT-1, rat glutamate transporter (EAAT2; slc1a2; Pines et al., 1992); GLUL, glutamine synthetase; TBOA, DL-threo-β-benzyloxyaspartate AbstractNeither normal brain function nor the pathological processes involved in neurological diseases can be adequately understood without knowledge of the release, uptake and metabolism of glutamate. The reason for this is that glutamate (a) is the most abundant amino acid in the brain, (b) is at the cross-roads between several metabolic pathways, and (c) serves as the major excitatory neurotransmitter. In fact most brain cells express glutamate receptors and are thereby influenced by extracellular glutamate. In agreement, brain cells have powerful uptake systems that constantly remove glutamate from the extracellular fluid and thereby limit receptor activation. It has been clear since the 1970s that astrocytes and neurons express glutamate transporters. The relative contribution of neuronal and glial transporters to the total glutamate uptake activity, however, as well as their functional importance, has been hotly debated ever since. The present short review provides (a) an overview of what we know about neuronal glutamate uptake as well as an historical description of how we got there, and (b) an hypothesis reconciling apparently contradicting observations thereby possibly resolving the paradox.

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“…EAAC1 is expressed in intestine, kidney, heart, lung, placenta and liver (Nakayama, Kawakami, Tanaka & Nakamura, 1996). Low levels of EAAT4 mRNA are found in placenta, and EAAT5 is expressed in liver, kidney, intestine, heart, lung and skeletal muscle (Gegelashvili et al, 1998, Lee, Anderson, Stevens, Beasley, Barnett & Pow, 2013). These differential expression patterns strongly suggest that each of these transporters is under specific transcriptional regulation.…”

Section: Differential Localization Of Glutamate Transportersmentioning

confidence: 99%

Transcriptional Regulation of Glutamate Transporters

Martínez-Lozada

Guillem

Robinson

2016

Advances in Pharmacology

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Glutamate is the predominant excitatory neurotransmitter in the mammalian CNS. It mediates essentially all rapid excitatory signaling. Dysfunction of glutamatergic signaling contributes to developmental, neurologic, and psychiatric disease. Extracellular glutamate is cleared by a family of five Na+-dependent glutamate transporters. Two of these transporters (GLAST and GLT-1) are relatively selectively expressed in astrocytes. Other of these transporters (EAAC1) is expressed by neurons throughout the nervous system. Expression of the last two members of this family (EAAT4 and EAAT5) is almost exclusively restricted to specific populations of neurons in cerebellum and retina, respectively. In this review, we will discuss our current understanding of the mechanisms that control transcriptional regulation of the different members of this family. Over the last two decades our understanding of the mechanisms that regulate expression of GLT-1 and GLAST has advanced considerably; several specific transcription factors, cis-elements, and epigenetic mechanisms have been identified. For the other members of the family, little or nothing is known about the mechanisms that control their transcription. It is assumed that by defining the mechanisms involved, we will advance our understanding of the events that result in cell specific expression of these transporters and perhaps begin to define the mechanisms by which neurologic diseases are changing the biology of the cells that express these transporters. This approach might provide a pathway for developing new therapies for a wide-range of essentially untreatable and devastating diseases that kill neurons by an excitotoxic mechanism.

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Excitatory Amino Acid Transporter 5 is widely expressed in peripheral tissues

Cited by 19 publications

References 27 publications

A novel splice variant of the Excitatory Amino Acid Transporter 5: Cloning, immunolocalization and functional characterization of hEAAT5v in human retina

A novel splice variant of the Excitatory Amino Acid Transporter 5: Cloning, immunolocalization and functional characterization of hEAAT5v in human retina

Neuronal vs glial glutamate uptake: Resolving the conundrum

Transcriptional Regulation of Glutamate Transporters

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