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COMP–Angiopoietin-1 Ameliorates Renal Fibrosis in a Unilateral Ureteral Obstruction Model

Won Kim^*, Sang-Ok Moon^*, Sang Yong Lee, Kyu Yun Jang, Chung-Hyun Cho, Gou Young Koh, Kyu-Sil Choi^||, Kwon-Ha Yoon^||, Mi Jeong Sung^*, Duk Hoon Kim^*, Sik Lee^*, Kyung Pyo Kang^* and Sung Kwang Park^*

^* Renal Regeneration Laboratory and Department of Internal Medicine, Department of Diagnostic Radiology, and Department of Pathology, Research Institute of Clinical Medicine, Chonbuk National University Medical School, Jeonju, Biomedical Research Center and Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, and ^|| Institute for Radiological Imaging Science, Wonkwang University School of Medicine, Iksan, South Korea

Address correspondence to: Dr. Sung Kwang Park, Renal Regeneration Laboratory and Department of Internal Medicine, Chonbuk National University Medical School, San 2-20 Keumam-dong, Jeonju, 561-180, South Korea. Phone: +82-63-250-1683; Fax: +82-63-254-1609; E-mail: parksk{at}chonbuk.ac.kr

Received for publication February 2, 2006. Accepted for publication June 25, 2006.

Injury to the renal microvasculature may be a major factor in the progression of renal disease; therefore, protection of endothelial cells (EC) in renal vasculature may have a therapeutic role in renal fibrosis. Recently, a soluble, stable, and potent angiopoietin-1 (Ang1) variant, cartilage oligomeric matrix protein (COMP)-Ang1, was developed. The contribution of COMP-Ang1 in renal interstitial fibrosis, however, remains to be clarified. This study investigated the effects of COMP-Ang1 on peritubular capillary EC in the renal cortex and the renal fibrogenic process that is triggered by unilateral ureteral obstruction. COMP-Ang1 preserved renal platelet-EC adhesion molecule-1–and Tie2-positive EC. Morphologic examination indicated less tubular injury and tubulointerstitial fibrosis in mice that received COMP-Ang1 than vehicle-treated mice. Interstitial type I collagen and myofibroblast accumulation were significantly suppressed by COMP-Ang1 treatment. COMP-Ang1 increased Tie2 and Akt phosphorylation in ureteral obstructed kidneys. Renal surface microvasculature and renal blood flow were higher after treatment with COMP-Ang1 than with vehicle. COMP-Ang1 treatment decreased monocyte/macrophage infiltration, tissue levels of TGF-1, and Smad 2/3 phosphorylation and increased Smad 7 in the obstructed kidney. These results demonstrate that COMP-Ang1 treatment can decrease the progression of renal fibrosis in unilateral ureteral obstruction. COMP-Ang1 may be an endothelium-specific therapeutic modality in fibrotic renal disease.

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