Changes in the expression of specific Müller cell proteins during long-term retinal detachment

Lewis, Geoffrey P.; Erickson, Page A.; Guérin, Christopher J.; Anderson, Don H.; Fisher, Steven K.

doi:10.1016/0014-4835(89)90079-1

Cited by 137 publications

(72 citation statements)

References 32 publications

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“…For example, the abundance of glutamine synthetase is increased 3 days after cerebellar lesions in fish , whereas this en-zyme is down-regulated under traumatic conditions in the mammalian central nervous system Hä rtig et al, 1995;Lewis et al, 1989Lewis et al, , 1994Oliver et al, 1990;Smith et al, 1991). Glutamine synthetase is a glia-specific enzyme that converts synaptically released glutamate into the nontoxic amino acid glutamine.…”

Section: Cns Of Teleost Fishmentioning

confidence: 99%

Stretching the limits: Stem cells in regeneration science

Stocum

Zupanc

2008

Developmental Dynamics

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Section: Cns Of Teleost Fishmentioning

confidence: 99%

Stretching the limits: Stem cells in regeneration science

Stocum

Zupanc

2008

Developmental Dynamics

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“…Müller cells, like astrocytes, up-regulate GFAP. In addition, both Müller glia cells and RPE cells can proliferate to form scar tissues within the retina [14]. They also can migrate into the vitreal space, proliferate, and form cellular membranes [7], a response known as proliferative vitreoretinopathy [11].…”

mentioning

confidence: 99%

Temporal regulation of CD81 following retinal injury in the rat

Song

Geisert

Vázquez-Chona

et al. 2003

Neuroscience Letters

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Following retinal injury, glial cells within the retina undergo a response that is characterized by the proliferation of astrocytes, Müller cells, and retinal pigment epithelial cells. CD81, a small membrane protein known to be involved in cell proliferation, is up-regulated after injury. This study focuses on the temporal regulation of CD81, relating the expression of this protein to glial fibrillary acidic protein (GFAP), the classic marker of gliosis. CD81 levels were elevated at 7 days after injury and remained elevated at 30 days after injury; GFAP was increased at 7 days and continued to increase until 30 days post injury. This association of CD81 with glial reactivity may provide a clue to the regulation of the proliferative response following retinal injury. KeywordsCD81; Glial fibrillary acidic protein; Retina; Injury; Tetraspanin; Gliosis; ProliferationThe response of the retina to trauma involves well-characterized cellular reactions [16], many of them similar to responses that occur in other parts of the central nervous system. As in the brain and spinal cord, a dramatic up-regulation of glial fibrillary acidic protein (GFAP) follows retinal injury. This up-regulation of GFAP marks reactive retinal astrocytes [12,16], which hypertrophy and increase their expression of the intermediate filament protein GFAP [3,13,18]. Müller glia and the retinal pigment epithelium (RPE), which are unique to the retina, also demonstrate characteristic responses to injury. Müller cells, like astrocytes, up-regulate GFAP. In addition, both Müller glia cells and RPE cells can proliferate to form scar tissues within the retina [14]. They also can migrate into the vitreal space, proliferate, and form cellular membranes [7], a response known as proliferative vitreoretinopathy [11]. These cellular membranes can then contract and cause secondary retinal detachments. The reactive glial responses and the proliferation of non-neuronal cells can have serious consequences, including loss of sight.Studies in our laboratory have identified a protein, CD81, which plays a role in the response of the brain [9], spinal cord [5], and retina [10]. We originally called CD81 the target of the antiproliferative antibody. As that name implies, this protein is part of a molecular complex that controls the proliferation of glial cells. We have hypothesized that this CD81 molecular complex is a key element in the contact inhibition between glial cells in the brain. Antibodies directed against CD81 depress the mitotic activity of cultured cells [9,17]. Furthermore, CD81 is expressed by glial cells in the brain during the second postnatal week, a time when their mitotic activity is down-regulated [19]. The antiproliferative role of this protein is confirmed by mice with a CD81-null mutation [10]. These CD81-null mice have very large brains containing an over abundance of astrocytes and microglia [10]. We have found that CD81 is In this study, we used the monoclonal antibody AMP1 to recognize CD81 [9]. A polyclonal antibody purchased from Li...

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“…This possibility is supported by the finding that an increase in GS expression in glial cells, caused by induction of its endogenous gene, has neuroprotective benefits (Gorovits et al 1997) and that GS expression and/or activity is down-regulated under certain neuropathological conditions (Lewis et al 1989;Oliver et al 1990;Smith et al 1991;Lewis et al 1994;Grosche et al 1995;Hartig et al 1995). We used the embryonic chicken retina for this study because the level of GS in this tissue can be closely regulated by glucocorticoids.…”

mentioning

confidence: 99%

Glutamine synthetase enhances the clearance of extracellular glutamate by the neural retina

Shaked

Ben-Dror

Vardimon

2002

Journal of Neurochemistry

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Clearance of synaptic glutamate by glial cells is required for the normal function of excitatory synapses and for prevention of neurotoxicity. Although the regulatory role of glial glutamate transporters in glutamate clearance is well established, little is known about the influence of glial glutamate metabolism on this process. This study examines whether glutamine synthetase (GS), a glial-specific enzyme that amidates glutamate to glutamine, affects the uptake of glutamate. Retinal explants were incubated in the presence of induction of the endogenous gene, did not affect the amount of glutamate accumulated within the cells, but led to a dramatic increase in the amount of glutamine released. This increase, which was directly correlated with the level of GS expression, was dependent on the presence of external sodium ions, and could be completely abolished by methionine sulfoximine, a specific inhibitor of GS activity. Our results demonstrate that GS activity significantly influences the uptake of glutamate by the neural retina and suggest that this enzyme may represent an important target for neuroprotective strategies.

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Changes in the expression of specific Müller cell proteins during long-term retinal detachment

Cited by 137 publications

References 32 publications

Stretching the limits: Stem cells in regeneration science

Stretching the limits: Stem cells in regeneration science

Temporal regulation of CD81 following retinal injury in the rat

Glutamine synthetase enhances the clearance of extracellular glutamate by the neural retina

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