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Intrarenal Injection of Bone Marrow-Derived Angiogenic Cells Reduces Endothelial Injury and Mesangial Cell Activation in Experimental Glomerulonephritis

Hideki Uchimura^*, Takeshi Marumo^,, Osamu Takase^*, Hiroshi Kawachi, Fujio Shimizu, Matsuhiko Hayashi^*, Takao Saruta^*, Keiichi Hishikawa^, and Toshiro Fujita^,

^* Department of Internal Medicine, Keio University School of Medicine, Tokyo; Department of Clinical Renal Regeneration and Division of Nephrology and Endocrinology, Department of Internal Medicine, University of Tokyo, Tokyo; and Department of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan

Address correspondence to: Dr. Takeshi Marumo, Department of Clinical Renal Regeneration, Division of Nephrology and Endocrinology, Department of Internal Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyouku, 113-8655 Tokyo, Japan. Phone: 81-3-3815-5411, ext. 35717; Fax: 81-3-5800-9738; E-mail: tmarumo-npr{at}umin.ac.jp

Received for publication May 10, 2004. Accepted for publication January 1, 2005.

Loss of glomerular endothelial cells has been suggested to contribute to the progression of glomerular injury. Although therapeutic angiogenesis induced by administration of bone marrow–derived endothelial progenitor cells has been observed in disease models of endothelial injury, the effects on renal disease have not been clarified. Whether administration of culture-modified bone marrow mononuclear cells would mitigate the glomerular endothelial injury in anti-Thy1.1 nephritis was investigated. After cultivation under conditions that promote endothelial progenitor cell growth, bone marrow mononuclear cells were labeled with CM-DiI, a fluorescence marker, and injected into the left renal artery of Lewis rats with anti-Thy1.1 glomerulonephritis. The decrease in glomerular endothelial cells was significantly attenuated in the left kidney, as compared with the right, in nephritic rats that received the cell infusion. Glomerular injury score, the area positive for mesangial -smooth muscle actin, and infiltration of macrophages were significantly decreased in the left kidney. CM-DiI–positive cells were distributed in glomeruli of the left kidney but not in those of the right kidney. Among CM-DiI–labeled cells incorporated into glomeruli, 16.5 ± 1.2% of cells were stained with an endothelial marker, rat endothelial cell antigen-1. Culture-modified mononuclear cells secreted 281.2 ± 85.0 pg of vascular endothelial growth factor per 10⁵ cells per day. In conclusion, intra-arterial administration of culture-modified bone marrow mononuclear cells reduced endothelial injury and mesangial activation in anti-Thy1.1 glomerulonephritis. Incorporation into the glomerular endothelial lining and production of angiogenic factor(s) are likely to contribute to the protective effects of culture-modified mononuclear cells against glomerular injury.

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