Chapter 9 gliosis of the mammalian retina: Migration and proliferation of retinal glia

Hjelmeland, Leonard M.

doi:10.1016/0278-4327(88)90011-9

Cited by 12 publications

(13 citation statements)

References 131 publications

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“…The Muller cell changes in the dystrophic retina are very similar to glial reaction to injury in the brain and retina (Harvey et al, 1987;Hjelmeland and Harvey, 1988;Lindsay, 1986). In the retina, reactive gliosis involves primarily Muller cells and astrocytes and occurs as early as the first week following injury.…”

Section: Discussionmentioning

confidence: 97%

Müller cell changes precede vascularization of the pigment epithelium in the dystrophic rat retina

Roque

Caldwell

1990

Glia

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In the Royal College of Surgeons rat with inherited retinal dystrophy, photoreceptor cell degeneration is accompanied by retinal pigment epithelial (RPE) cell alterations and Müller cell changes such as increased expression of glial fibrillary acidic protein (GFAP). Vascular changes such as vascularization of the RPE, vascular proliferation, and formation of vitreoretinal membranes (VRMs) are observed later. To study the relationship of Müller cell changes to the vascular alterations in the dystrophic retina, we used immunoperoxidase techniques and antibodies against GFAP and vimentin. Our study showed that during photoreceptor degeneration, Müller cells expressed small amounts of GFAP. As degeneration progressed, GFAP expression increased and morphological alterations occurred in Müller cells. Müller cell apical processes extended and proliferated in the subretinal space and contacted the apical surface of duplicated RPE cells. Later, GFAP reactive fibers surrounded retinal vessels apposed to the RPE. As the vessels became enmeshed within the RPE, the GFAP-positive perivascular processes disappeared. Eventually, the RPE-associated vessels became displaced into the inner retina where VRMs were sometimes observed. Immunoblots showed increased GFAP in dystrophic as compared with control retinas. Studies of vimentin distribution in the dystrophic retina showed results similar to the GFAP study. Moreover, the vimentin study suggested increased number of Müller cell processes in the dystrophic as compared with control retinas. The close temporal and anatomical relationships among Müller cell, RPE, and vascular changes in the dystrophic rat suggest a role for Müller cells in retinal neovascularization and proliferative retinopathy.

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Section: Discussionmentioning

confidence: 97%

Müller cell changes precede vascularization of the pigment epithelium in the dystrophic rat retina

Roque

Caldwell

1990

Glia

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“…One interpretation of this result is that neuronal death induced Thy-1 expression in another cell type. Muller cells are the main glial cell type present in the retina, and they respond to injury and disease by undergoing a series of morphological and biochemical changes, including changes in protein expression (Hjelmeland and Harvey, 1988). This led us to investigate whether Thy-1 could be expressed by Muller cells.…”

Section: Discussionmentioning

confidence: 99%

Rat retinal müller cells express Thy‐1 following neuronal cell death

Dabin

Barnstable

1995

Glia

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In the normal rat retina the Thy-1 antigen is a specific marker of ganglion cells, but degeneration of ganglion cells in vivo does not remove completely the expression of Thy-1 in the retina. To reconcile these differences we have postulated that ganglion cell death could induce a glial response including the expression of Thy-1 in Müller cells, the main glial cell type in the retina. Using immunocytochemistry, we have shown that pure cultures of Müller cells were strongly labelled with antibodies against Thy-1. PCR amplification of cDNA reverse transcribed from Müller cell RNA indicated the presence of Thy-1 transcripts. Double labelling experiments with anti-Thy1 and anti-glutamine synthetase, a marker of Müller cells, indicated the presence of both antigens in the same cells. Although Müller cells expressed Thy-1 mRNA and protein when cultured in the absence of neuronal cells, when co-cultured with retinal neurons they were not labelled with antibodies against Thy-1. Our results suggest that Thy-1 is expressed by Müller cells following loss of retinal neurons. Thy-1 may have an important function during glial response to neuron death in retina.

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“…In particu lar, the temporal quadrant displayed the strongest GFAP staining and the highest pho toreceptor loss as well as scar formation. In this quadrant, reactive gliosis [23] ed to horizontally oriented glial processes [24] and not to horizontal cell processes. The ram ifications of horizontal cells are situated proximally to the residual ONL and are not la belled.…”

Section: Discussionmentioning

confidence: 99%

Light Damage in the Rat Retina: Glial Fibrillary Acidic Protein Accumulates in Müller Cells in Correlation with Photoreceptor Damage

Raad¹,

Szczęsny

Munz

et al. 1996

Ophthalmic Res

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Low intensity diffuse white fluorescent light (1,000 1x for 2 h) exclusively induced photoreceptor damage in the inferior retina of albino rats; the temporal retina showed extensive damage, whereas the nasal retina revealed threshold lesions prior to recovery. To expand our morphological data, further experiments were undertaken to determine if glial fibrillary acidic protein (GFAP) expression was associated with the regions of photoreceptor damage. To follow the time course of GFAP expression, immunoblot analysis was carried out on retinal homogenates of dark-adapted (control) rats and light-exposed rats returned to cyclic light for 0 h, 1, 2, 3 and 6 days. A significant twofold increase in GFAP immunoreactivity over controls was observed in the retinas of light-exposed rats returned to cyclic light for 6 days. Using an indirect immunohistochemical method, retinal sections of the control and light-exposed rats allowed to recover for 6 days were stained for GFAP. GFAP immunoreactivity was localised to the astrocytes and Müller cells. Moreover, GFAP staining in Müller cells in the retinas of control animals was uniformly restricted to rare end-feet. In contrast, a gradient of GFAP immunoreactivity was observed in experimental rats, rising from the superior retina to the inferior temporal quadrant; the GFAP staining in the inferior nasal quadrant was intermediate. Thus, GFAP immunoreactivity was proportional to photoreceptor damage. Interestingly, no GFAP induction could be demonstrated in the pineal glands of light-exposed rats.

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Chapter 9 gliosis of the mammalian retina: Migration and proliferation of retinal glia

Cited by 12 publications

References 131 publications

Müller cell changes precede vascularization of the pigment epithelium in the dystrophic rat retina

Müller cell changes precede vascularization of the pigment epithelium in the dystrophic rat retina

Rat retinal müller cells express Thy‐1 following neuronal cell death

Light Damage in the Rat Retina: Glial Fibrillary Acidic Protein Accumulates in Müller Cells in Correlation with Photoreceptor Damage

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