[Expression of Mn-SOD mRNA in streptozotocin-induced diabetic rat cornea by in situ hybridization].
The pathogenesis of diabetic corneal epitheliopathy, one of the ocular complications frequently seen in diabetes patients, still remains to be elucidated. Hyperglycemia causes glycation of various proteins leading to the formation of superoxide radicals (O2.-). Copper, zinc-superoxide dismutase (Cu, Zn-SOD), a scavenger of superoxide radicals, whose function is complementary to manganese-SOD (Mn-SOD), is inactivated during glycation. As a first step to clarify whether depressed antioxidant activity is associated with diabetic corneal epitheliopathy or not, we investigated the expression of Mn-SOD mRNA (messenger ribonuclic acid) in streptozotocin-induced diabetic rat cornea by in situ hybridization using a digoxigenin-labeled Mn-SOD cDNA probe. Mn-SOD mRNA was detected in epithelial cell layer and endothelial cell layer of both diabetic rat cornea and normal rat cornea. However, the expression of Mn-SOD mMRA in the epithelial cell layer of diabetic rat cornea was weaker than that of normal rat cornea. These results suggest that decreased Mn-SOD activity might be one of factors causing diabetic corneal epitheliopathy.
Beppu
H
H
Department of Ophthalmology, Kobe University, School of Medicine, Hyougo-ken, Japan.
Nakamura
M
M
Katakami
C
C
Yamamoto
M
M
D000818:Animals; D003316:Corneal Diseases / Q000209:etiology*; D003921:Diabetes Mellitus, Experimental / Q000150:complications*; D004728:Endothelium, Corneal / Q000201:enzymology; D017403:In Situ Hybridization; D008297:Male; D012333:RNA, Messenger / Q000032:analysis*; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin; D013482:Superoxide Dismutase / Q000378:metabolism*
D012333:RNA, Messenger; D013311:Streptozocin; D013482:Superoxide Dismutase