Developmental expression of the Glial fibrillary acidic protein (GFAP) gene in the mouse retina

Sarthy, P. Vijay; Fu, Marlene; Huang, Jing

doi:10.1007/bf00741450

Cited by 61 publications

(54 citation statements)

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“…In the retina, neuroligin expression is located in the GFAP-positive astrocytes, which are found only in the ganglion cell and nerve fiber layers. GFAP-positive retinal astrocytes migrate from the optic stalk into the retina starting at about postnatal day 1 in the mouse (Sarthy et al, 1991). At early postnatal stages, neuroligin expression is found associated with the GFAP-positive processes of the astrocytes in the honeycomb-like array of glial processes that surround the ganglion cells and in the lamina propria of the retinal nerve layer (Fig.…”

Section: Discussionmentioning

confidence: 96%

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Neuroligin 3 is a vertebrate gliotactin expressed in the olfactory ensheathing glia, a growth‐promoting class of macroglia

Gilbert

Smith

Roskams

et al. 2001

Glia

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The molecular mechanisms that drive glia-glial interactions and glia-neuronal interactions during the development of the nervous system are poorly understood. A number of membrane-bound cell adhesion molecules have been shown to play a role, although the precise nature of their involvement is unknown. One class of molecules with cell adhesive properties used in the nervous system is the serine-esterase-like family of transmembrane proteins. A member of this class, a glia-specific protein called gliotactin, has been shown to be necessary for the development of the glial sheath in the peripheral nervous system of Drosophila melanogaster. Gliotactin is essential for the development of septate junctions in the glial sheath of individual and neighboring glia. Mutations that remove this protein result in paralysis and eventually death due to a breakdown in the glial-based blood-nerve barrier. To study the role of gliotactin during vertebrate nervous system development, we have isolated a potential vertebrate gliotactin homologue from mice and rat and found that it corresponds to neuroligin 3. Using a combination of RT-PCR and immunohistochemistry, we have found that neuroligin 3 is expressed during the development of the nervous system in many classes of glia. In particular neuroligin 3 is expressed in the olfactory ensheathing glia, retinal astrocytes, Schwann cells, and spinal cord astrocytes in the developing embryo. This expression is developmentally controlled such that in postnatal and adult stages, neuroligin 3 continues to be expressed at high levels in the olfactory ensheathing glia, a highly plastic class of glia that retain many of their developmental characteristics throughout life.

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Section: Discussionmentioning

confidence: 96%

“…The astrocytes originate in the optic stalk and invade the retina starting after birth (Huxlin et al, 1992;Ling et al, 1989). In the P5 retina, the astrocytes which are found in the outer plexiform layer (OPL) and optic nerve fiber layer (ONFL) stain for GFAP (Sarthy et al, 1991) (Fig. 5A).…”

Section: Neuroligin 3 Is Expressed In Retinal Astrocytesmentioning

confidence: 99%

Neuroligin 3 is a vertebrate gliotactin expressed in the olfactory ensheathing glia, a growth‐promoting class of macroglia

Gilbert

Smith

Roskams

et al. 2001

Glia

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“…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.…”

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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“…Healthy retinal tissue does not express GFAP in its muller cells tissue layer. Thus a correlation is suggested between GFAP expression and damaged muller cell tissue in the retina [20,21].…”

Section: Journal Of Clinical and Experimental Ophthalmologymentioning

confidence: 99%

In Vitro Biocompatibility of Silicone Oil Siluron Xtra® on Porcine Retina in a Perfusion Culture System

Neuer¹,

Bohnacker²,

Feucht³

et al. 2017

J Clin Exp Ophthalmol

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Developmental expression of the Glial fibrillary acidic protein (GFAP) gene in the mouse retina

Cited by 61 publications

References 50 publications

Neuroligin 3 is a vertebrate gliotactin expressed in the olfactory ensheathing glia, a growth‐promoting class of macroglia

Neuroligin 3 is a vertebrate gliotactin expressed in the olfactory ensheathing glia, a growth‐promoting class of macroglia

Temporal regulation of CD81 following retinal injury in the rat

In Vitro Biocompatibility of Silicone Oil Siluron Xtra® on Porcine Retina in a Perfusion Culture System

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