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J Am Soc Nephrol 14:1559-1567, 2003
© 2003 American Society of Nephrology

BMP-7 Is an Efficacious Treatment of Vascular Calcification in a Murine Model of Atherosclerosis and Chronic Renal Failure

Matthew R. Davies*,{dagger}, Richard J. Lund{dagger} and Keith A. Hruska*,{dagger},{ddagger}

Renal Divisions, *Departments of Pediatrics, {dagger}Internal Medicine, and {ddagger}Cell Biology, Washington University School of Medicine, St. Louis, Missouri.

Correspondence to Dr. Keith A. Hruska, Department of Pediatrics & Renal Division, Washington University School of Medicine,, McDonnell Pediatric Research Building, 660 S Euclid Avenue, Campus Box 8208, St Louis, MO 63110. Phone: 314-286-2772; Fax: 314-286-2894;

ABSTRACT. Chronic renal failure is complicated by high cardiovascular mortality. One key contributor to this mortality is vascular calcification, for which no therapy currently exists. Bone morphogenetic protein 7 is an essential renal morphogen that maintains renal tubular differentiation in the adult and is downregulated in renal failure. Several studies have demonstrated its efficacy in treating various renal diseases in rodents, and it was hypothesized that it would also be an effective treatment of vascular calcification in this setting. Uremia was imposed on LDL receptor null mice (a model of atherosclerosis), which were then treated with bone morphogenetic protein 7 for 15 wk. Uremic animals had increased vascular calcification by histology and chemical analysis. Calcification in treated animals was similar to or less than non-uremic control animals. Cells exhibiting an osteoblast-like phenotype in the vessel wall may be important in the etiology of vascular calcification. Expression of osteocalcin was assessed as a marker of osteoblastic function, and it is shown that it is increased in untreated uremic animals but downregulated to levels similar to non-uremic control animals with treatment. The data are compatible with bone morphogenetic protein 7 deficiency as a pathophysiologic factor in chronic renal failure, and they demonstrate its efficacy as a potential treatment of vascular calcification. E-mail: hruska_k@kids.wustl.edu




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