Retinal heat shock protein 25 in early experimental diabetes

Diabetic retinopathy is the leading cause of blindness in adults, and oxidative stress has been pathogenically associated with retinal neurodegeneration. Cellular stresses induce expression of heat shock proteins (HSPs) and this results in cytoprotection. Our aim was to assess retinal expression of...

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Bibliographic Details
Published in:Acta diabetologica 2013-08, Vol.50 (4), p.579-585
Main Authors: Pinach, Silvia, Burt, Davina, Berrone, Elena, Barutta, Federica, Bruno, Graziella, Porta, Massimo, Perin, Paolo Cavallo, Gruden, Gabriella
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Diabetes
Diabetes Mellitus, Experimental - complications
Diabetes Mellitus, Experimental - genetics
Diabetes Mellitus, Experimental - metabolism
Diabetes Mellitus, Experimental - physiopathology
Diabetic retinopathy
Diabetic Retinopathy - genetics
Diabetic Retinopathy - metabolism
Diabetic Retinopathy - physiopathology
Female
Heat shock proteins
Heat-Shock Proteins - genetics
Heat-Shock Proteins - metabolism
Humans
Internal Medicine
Male
Medicine
Medicine & Public Health
Metabolic Diseases
Mice
Mice, Inbred C57BL
Neoplasm Proteins - genetics
Neoplasm Proteins - metabolism
Original Article
Oxidative Stress
Retina - cytology
Retina - metabolism
Retinal Ganglion Cells - cytology
Retinal Ganglion Cells - metabolism
Up-Regulation
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Summary:Diabetic retinopathy is the leading cause of blindness in adults, and oxidative stress has been pathogenically associated with retinal neurodegeneration. Cellular stresses induce expression of heat shock proteins (HSPs) and this results in cytoprotection. Our aim was to assess retinal expression of HSP25 in early experimental diabetes. Mice were rendered diabetic by streptozotocin injection. Ten weeks after diabetes onset retinal HSP25 expression were studied by real-time PCR, immunoblotting and immunohistochemistry (IHC). Expression of nitrotyrosine and Cu/Zn superoxide dismutase (SOD), was assessed by IHC and apoptosis by TUNEL. Retinal HSP25 mRNA and protein expression was significantly increased in diabetic as compared to non-diabetic animals and localised predominantly within the retinal ganglion cells (RGC) layer. This was paralleled overexpression of nitrotyrosine and SOD and enhanced apoptosis. In early experimental diabetes, HSP25 is overexpressed in the RGC layer in parallel with markers of oxidative stress and apoptosis.
ISSN:0940-5429
1432-5233
DOI:10.1007/s00592-011-0346-1