Receptor for advanced glycation end product expression in experimental diabetic retinopathy.
The advanced glycation end product (AGE)-receptor for AGE (RAGE) pathway is involved in the pathogenesis of diabetic microvascular damage. The special distribution of RAGE and its engagement has an impact on the development of diabetic retinopathy. In the present study, we used immunofluorescence and confocal laser microscopy to study RAGE expression with special emphasis on Müller glia in Sprague Dawley rats. RAGE expression was low in nondiabetic retinae and was found in ganglion cells and Müller cell end feet. In diabetic retinae, upregulated RAGE was predominantly expressed in retinal glia. Since Müller cells are important in the regulation of important features of early retinal vascular damage, such as vascular permeability, homeostasis, and response to stress, RAGE appears to be a central modulator in diabetic retinopathy.
Wang
Yumei
Y
5th Medical Clinic, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
Vom Hagen
Franziska
F
Pfister
Frederick
F
Bierhaus
Angelika
A
Feng
Yuxi
Y
Gans
Reinhold
R
Hammes
Hans-Peter
HP
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D003930:Diabetic Retinopathy / Q000378:metabolism*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism*; D012016:Reference Values; D012160:Retina / Q000378:metabolism / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000378:metabolism
D005904:Glial Fibrillary Acidic Protein; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic