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J Am Soc Nephrol 12:2721-2731, 2001
© 2001 American Society of Nephrology

Increased Renal Angiopoietin-1 Expression in Folic Acid-Induced Nephrotoxicity in Mice

David A. Long*, Adrian S. Woolf*, Toshio Suda{dagger} and Hai T. Yuan*

*Nephro-Urology Unit, Institute of Child Health, University College London, London, United Kingdom; and {dagger}Department of Cell Differentiation, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, Kumamoto, Japan.

Correspondence to Dr. Hai T. Yuan, Nephro-Urology Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK. Phone: 00-44-207-905-2196; Fax: 00-44-207-916-0011; E-mail: h.yuan{at}ich.ucl.ac.uk

ABSTRACT. Growth factors affect epithelial regeneration after acute renal injury, but less is known regarding the expression of vascular growth factors in this setting. A mouse model of folic acid (FA)-induced nephrotoxicity was used to study the expression of angiopoietins (Ang), factors that bind the Tie-2 receptor and modulate endothelial growth. Tubular damage was detected 1 d after FA administration; in the next 14 d, most tubules regenerated but patchy atrophy, with interstitial fibrosis, was also observed. Ang-1 immunostaining was detected between cortical tubules and in the vasa rectae of vehicle-treated animals. FA-induced nephropathy was associated with the acquisition of Ang-1 immunostaining in renal arterial walls and in a subset of injured cortical tubules that failed to stain with periodic acid-Schiff stain, which indicated that they were distal tubules. Renal Ang-1 protein levels were significantly increased after FA administration, compared with time-matched control values, as assessed by Western blotting. Capillaries between regenerating tubules expressed both Tie-2 and platelet-endothelial cell adhesion molecule. A subset of these endothelia expressed proliferating cell nuclear antigen, whereas capillary proliferation was absent in control samples. Therefore, FA-induced nephropathy is associated with increased Ang-1 protein expression in renal epithelia and arteries. In addition, Tie-2-expressing capillaries near damaged cortical tubules undergo proliferation. Further experiments are required to establish whether these events are functionally related.




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