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Anne M. Haapaniemi, Andrey A. Nedorubov, Giedrius Kalesnykas, Stanislav I. Shram; Twelve-week Streptozotocin-induced Diabetes In Rats Does Not Cause Significant Retinal Degeneration, But Upregulates Heat Shock Protein Response. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5400.
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To evaluate cellular stress response and neurodegeneration in the streptozotocin-induced rat model of diabetes mellitus.
Insulin-dependent diabetes in male Wistar rats (220-250 g) was caused by single i.p. injection of streptozotocin (60 mg/kg). Only animals with glucose blood concentration >20 mmol/l were taken for further investigations. After 12 weeks the animals were sacrificed and the eyes as well as the optic nerves were processed for histology and immunohistochemistry. The paraffin-embedded retinal sections were stained for heat shock protein 27kDa (Hsp27), 60 kDa (Hsp60), 70 kDa (Hsp70), 90 kDa (Hsp90), and hypoxia-inducible factor 1α (Hif1α). Silver staining of the optic nerve sections and TUNEL staining of retinal sections were performed to evaluate axon damage and apoptosis in the retinal ganglion cell layer (RGCL). Retinal astrocytes with activated Müller cells were detected using antibody against glial fibrillary acidic protein (GFAP) and Iba1.
Twelve-week diabetes caused a significant increase in GFAP immunoreactivity in the retina. We did not find an increase in the number of apoptotic cells in RGCL or an increased degeneration in the optic nerve. However, all Hsps tested were upregulated in retinas of diabetic rats with varying degrees: from weak (Hsp60 and Hsp70) to moderate (Hsp90 and Hif1a) and strong (Hsp27) immunoreactivity of retina.
Twelve-week streptozotocin-induced diabetes causes cellular stress in retinal neurons without noticeable neuronal damage.
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