Muller's Cell Involvement in Proliferative Diabetic Retinopathy

Nork, T. Michael; Wallow, Ingolf H. L.; Sramek, Stephen J.; Anderson, Garth R.

doi:10.1001/archopht.1987.01060100126042

Cited by 107 publications

(55 citation statements)

References 23 publications

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“…The retinal glial cells have a multitude of roles for retinal maintenance and function, ranging from involvement in retinal metabolism (Newman 1987), endocrine functions (Berka et al 1995), and importance for the structural development of the retina (Tout et al 1993). Furthermore, retinal glial cells proliferate in response to retinal injury in general as well as to specific mitogens (Puro et al 1990), and these cells are strongly involved in the formation of epiretinal membranes in proliferative vitreoretinopathy (Nork et al 1987;Hosoda et al 1993). Future studies will show whether the present finding of glial cell invasion into retinal vessels can point towards new experimental approaches for elucidating the pathophysiology of retinal disease, notably vascular occlusion in diabetic retinopathy.…”

Section: Discussioncontrasting

confidence: 39%

Glial cell involvement in vascular occlusion of diabetic retinopathy

Bek

1997

Acta Ophthalmologica Scandinavica

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ABSTRACT. Twenty areas of retinal vascular occlusion from ten eyes of 6 diabetic patients were studied by immunohistochemistry to type IV collagen (basement membranes), von Willebrand factor (endothelial cells), and to glial fibrillary acid protein (glial cells) on serial sections. In all studied lesions immunoreactivity to type IV collagen and von Willebrand factor was confined to the retinal vascular walls whereas the material accumulated to occlude the vascular lumens centrally displayed immunoreactivity to glial fibrillary acid protein. All arterioles observed in the lesions were occluded. These arterioles had retained their circular shape, and the intravascular glial protein immunoreactivity communicated with the extravascular glial tissue through localised breaks in the vascular wall. The intravascular immunoreactivity was found to continue inside the arteriole along its successive diminishing to reach the capillary level. The venules were only occluded in less than half of the studied lesions. These venules were collapsed to assume a bean-like shape, and sequences with total obliteration of the vascular lumen alternated with sequences where a residual space corresponding to the former lumen displayed immunoreactivity to glial protein. The paper suggests that glial cell invasion, but not endothelial cells or basement membrane thickening, occludes the vascular lumen in areas of retinal non-perfusion secondary to diabetic retinopathy.

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Section: Discussioncontrasting

confidence: 39%

Glial cell involvement in vascular occlusion of diabetic retinopathy

Bek

1997

Acta Ophthalmologica Scandinavica

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“…12 In the present study, we found in both sham and untreated ROP rats, that both AT1 and AT2 receptors were localized not only to blood vessels but also to the ILM and nuclei in the INL, which presumably represent macroglial Muller cells. Importantly, Muller cells are associated with retinal blood vessels 47 and are sites of VEGF and VEGF-R2 expression. 7,25,48 It is therefore possible that ANG II via the AT2 receptor may influence retinal angiogenesis via a paracrine effect on VEGF in certain cells that support the retinal microvasculature.…”

Section: Discussionmentioning

confidence: 45%

Retinal Angiogenesis Is Mediated by an Interaction between the Angiotensin Type 2 Receptor, VEGF, and Angiopoietin

Sarlos

Rizkalla

Moravski

et al. 2003

The American Journal of Pathology

131

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There is evidence that angiotensin II, vascular endothelial growth factor (VEGF), angiopoietins, and their cognate receptors participate in retinal angiogenesis. We investigated whether angiotensin type 2-receptor blockade (AT2-RB) reduces retinal angiogenesis and alters the expression of VEGF/VEGF-R2 and angiopoietin-Tie2. Retinopathy of prematurity (ROP) was induced in Sprague Dawley (SD) rats by exposure to 80% oxygen from postnatal (P) days 0 to 11, followed by 7 days in room air. ROP shams were in room air from P0 -18. A group of ROP rats received the AT2-RB, PD123319, by mini-osmotic pump (5 mg/kg/day) from P11-18 (angiogenesis period). Evaluation of the retinal status of the AT2 receptor indicated that this receptor, as assessed by real-time PCR, immunohistochemistry, and in vitro autoradiography, was present in the retina, was more abundant than the AT1 receptor in the neonatal retina, and was increased in the ROP model. AT2-RB reduced retinal angiogenesis. VEGF and VEGF-R2 mRNA were increased in ROP and localized to blood vessels, ganglion cells, and the inner nuclear layer, and were decreased by PD123319. Angiopoietin2 and Tie2, but not angiopoietin1 mRNA were increased with ROP, and angiopoietin2 was reduced with PD123319. This study has identified a potential retinoprotective role for AT2-RB possibly mediated via interactions with VEGF-and angiopoietin-dependent pathways.

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“…semble the changes documented in other retinal disorders (Nork et al, 1987). It has been suggested that separation of neural retina from the retinal pigment epithelium initiated a number of cellular and biochemical changes within the retina (Hjelmeland and Harvey, 1988;Fisher and Anderson, 1989).…”

Section: Discussionsupporting

confidence: 41%

Dysfunction of Retinal Cell and Optic Nerve by Continuous Cerebroventricular Infusion of Glucosamine

Jang¹,

Han

Jun

et al. 2009

Biomolecules and Therapeutics

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-We have investigated the effect of glucosamine on the retinal cells after continuous infusion into cerebroventricle by using osmotic minipump to avoid peripheral effect. Continuous intracerebroventricular (i.c.v) infusion of glucosamine with the rate of 0.1 μmol/10 μl/hr for 7 days resulted in morphological changes of the optic nerve in electron microscopic level as well as morphological changes of the retina in light microscopic level. Retinal sections were immunostained for the detection of morphological changes of astrocytes. GFAP immunoreactivity appeared not only in the Muller cells but also many of the radial processes of Muller cells. The optic nerve showed deformed axon and slight lamellar separation of myelin sheath after continuous infusion of glucosamine in observing with electron microscope. Interestingly, vacuoles were observed in deformed axons and retinal layers were folded and detached. These results suggested that glucosamine plays a role in induction of morphological dysfunction in retina and optic nerves.

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Muller's Cell Involvement in Proliferative Diabetic Retinopathy

Cited by 107 publications

References 23 publications

Glial cell involvement in vascular occlusion of diabetic retinopathy

Glial cell involvement in vascular occlusion of diabetic retinopathy

Retinal Angiogenesis Is Mediated by an Interaction between the Angiotensin Type 2 Receptor, VEGF, and Angiopoietin

Dysfunction of Retinal Cell and Optic Nerve by Continuous Cerebroventricular Infusion of Glucosamine

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