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J Am Soc Nephrol 15:2125-2138, 2004
© 2004 American Society of Nephrology

BASIC SCIENCE

Accelerated Nephropathy in Diabetic Apolipoprotein E-Knockout Mouse: Role of Advanced Glycation End Products

Markus Lassila*, Kwee K. Seah*, Terri J. Allen*, Vicki Thallas*, Merlin C. Thomas*, Riccardo Candido*, Wendy C. Burns*, Josephine M. Forbes*, Anna C. Calkin{dagger}, Mark E. Cooper* and Karin A.M. Jandeleit-Dahm*

*Danielle Alberti Memorial Centre for Diabetes Complications, Vascular Division, Wynn Domain, Baker Heart Research Institute, Melbourne, Victoria, Australia; and {dagger}Department of Medicine, Central and Eastern Clinical School, Monash University, Alfred Hospital, Melbourne, Australia

Correspondence to Dr. Karin A.M. Jandeleit-Dahm, Baker Heart Research Institute, PO Box 6492, Commercial Road, Melbourne 8008, VIC 3004, Australia. Phone: +61-3-9276-2983; Fax: +61-3-8532-1288; E-mail: karin.jandeleit-dahm{at}baker.edu.au

ABSTRACT. Hyperlipidemia not only may be relevant to cardiovascular disease in diabetes but may also play a role in the development and progression of diabetic nephropathy. Furthermore, there is increasing evidence that advanced glycation end products (AGE) play an important role in diabetic renal disease. The objectives of this study were first to characterize renal injury in diabetic apolipoprotein E knockout (apo E-KO) mice and second to explore the role of AGE in the development and progression of renal disease in this model. Diabetes was induced by injection of streptozotocin in 6-wk-old apo E-KO mice. Diabetic animals received no treatment or treatment with the inhibitor of AGE formation aminoguanidine (1 g/kg per d) or the cross-link breaker [4,5-dimethyl-3-(2-oxo2-phenylethyl)-thiazolium chloride] ALT-711, which cleaves preformed AGE (20 mg/kg per d) for 20 wk. Nondiabetic apo E-KO mice as well as nondiabetic and diabetic C57BL/6 mice served as controls. Compared with nondiabetic apo E-KO mice, induction of diabetes in apo E-KO mice resulted in accelerated renal injury characterized by albuminuria and glomerular and tubulointerstitial injury. These abnormalities were associated with increased expression of collagen type I and type IV and transforming growth factor-{beta}1 (TGF-{beta}1), increased {alpha}-smooth muscle actin immunostaining and macrophage infiltration, and increased serum and renal AGE. The two treatments, which attenuated renal AGE accumulation in a disparate manner, were associated with less albuminuria, structural injury, macrophage infiltration, TGF-{beta}1, and collagen expression. The accelerated renal injury that was observed in diabetic apo E-KO mice was attenuated by approaches that inhibit renal AGE accumulation.




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