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Glial reactivity, an early feature of diabetic retinopathy.
Invest Ophthalmol Vis Sci. 2000 Jun; 41(7):1971-80.IO

Abstract

PURPOSE

To characterize early structural gliotic reactions in retinal Müller cells, astrocytes, and microglia in experimentally induced diabetes.

METHODS

Rats were rendered diabetic by streptozotocin injection and killed after 2, 4, 12, or 20 weeks. Cell densities were determined in flatmounted retinas or transverse semithin sections. Expression of glial fibrillary acidic protein (GFAP) was localized on frozen sections or flatmounts by immunofluorescence and confocal microscopy, and GFAP content was evaluated by Western blot analysis. Microglial cells were visualized by binding of isolectin B4 or staining with antibodies to phosphotyrosine residues. The integrity of the blood-retinal barrier was assessed by intravenous injection of Evans blue.

RESULTS

The density of Müller cells and microglia was significantly increased at 4 weeks of diabetes compared with nondiabetic controls. GFAP expression in Müller cells was not detected at 4 weeks but was prominent at 12 weeks. The number of astrocytes was significantly reduced at 4 weeks in the peripapillary and far peripheral retina. Shape changes of microglial cells indicated functional activation. Leakage of the blood-retinal barrier was observed at 2 weeks of hyperglycemia, the earliest time point investigated.

CONCLUSIONS

The leakage of the blood-retinal barrier before glial reactivity suggests that glia are early targets of vascular hyperpermeability. The individual glial cell types react differentially to the diabetic state. Müller cells undergo hyperplasia preceding GFAP expression, and microglial cells are activated, whereas astrocytes regress. This glial behavior may contribute decisively to the onset and development of neuropathy in the diabetic retina.

Authors+Show Affiliations

Cell Biology Laboratory, University Eye Clinic, Geneva, Switzerland. elisabeth.rungger@hcuge.chNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10845624

Citation

Rungger-Brändle, E, et al. "Glial Reactivity, an Early Feature of Diabetic Retinopathy." Investigative Ophthalmology & Visual Science, vol. 41, no. 7, 2000, pp. 1971-80.
Rungger-Brändle E, Dosso AA, Leuenberger PM. Glial reactivity, an early feature of diabetic retinopathy. Invest Ophthalmol Vis Sci. 2000;41(7):1971-80.
Rungger-Brändle, E., Dosso, A. A., & Leuenberger, P. M. (2000). Glial reactivity, an early feature of diabetic retinopathy. Investigative Ophthalmology & Visual Science, 41(7), 1971-80.
Rungger-Brändle E, Dosso AA, Leuenberger PM. Glial Reactivity, an Early Feature of Diabetic Retinopathy. Invest Ophthalmol Vis Sci. 2000;41(7):1971-80. PubMed PMID: 10845624.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glial reactivity, an early feature of diabetic retinopathy. AU - Rungger-Brändle,E, AU - Dosso,A A, AU - Leuenberger,P M, PY - 2000/6/14/pubmed PY - 2000/6/17/medline PY - 2000/6/14/entrez SP - 1971 EP - 80 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 41 IS - 7 N2 - PURPOSE: To characterize early structural gliotic reactions in retinal Müller cells, astrocytes, and microglia in experimentally induced diabetes. METHODS: Rats were rendered diabetic by streptozotocin injection and killed after 2, 4, 12, or 20 weeks. Cell densities were determined in flatmounted retinas or transverse semithin sections. Expression of glial fibrillary acidic protein (GFAP) was localized on frozen sections or flatmounts by immunofluorescence and confocal microscopy, and GFAP content was evaluated by Western blot analysis. Microglial cells were visualized by binding of isolectin B4 or staining with antibodies to phosphotyrosine residues. The integrity of the blood-retinal barrier was assessed by intravenous injection of Evans blue. RESULTS: The density of Müller cells and microglia was significantly increased at 4 weeks of diabetes compared with nondiabetic controls. GFAP expression in Müller cells was not detected at 4 weeks but was prominent at 12 weeks. The number of astrocytes was significantly reduced at 4 weeks in the peripapillary and far peripheral retina. Shape changes of microglial cells indicated functional activation. Leakage of the blood-retinal barrier was observed at 2 weeks of hyperglycemia, the earliest time point investigated. CONCLUSIONS: The leakage of the blood-retinal barrier before glial reactivity suggests that glia are early targets of vascular hyperpermeability. The individual glial cell types react differentially to the diabetic state. Müller cells undergo hyperplasia preceding GFAP expression, and microglial cells are activated, whereas astrocytes regress. This glial behavior may contribute decisively to the onset and development of neuropathy in the diabetic retina. SN - 0146-0404 UR - https://www.unboundmedicine.com/medline/citation/10845624/Glial_reactivity_an_early_feature_of_diabetic_retinopathy_ L2 - https://iovs.arvojournals.org/article.aspx?volume=41&issue=7&page=1971 DB - PRIME DP - Unbound Medicine ER -