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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 297/4/F952    most recent 00064.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Jung, Y. J. Articles by Kim, W. PubMed PubMed Citation Articles by Jung, Y. J. Articles by Kim, W.

Peritubular capillary preservation with COMP-angiopoietin-1 decreases ischemia-reperfusion-induced acute kidney injury

¹Renal Regeneration Laboratory and Department of Internal Medicine, ; ²Department of Diagnostic Radiology, and ; ³Department of Pathology, Research Institute of Clinical Medicine, Chonbuk National University Medical School, Jeonju; and ; ⁴Food Function Research Center, Korea Food Research Institute, Songnam, South Korea

Submitted February 6, 2009 ; accepted in final form August 2, 2009

Ischemia followed by reperfusion induces microvascular endothelial cell injury, leading to the loss of functions such as regulation of vascular tone, tissue perfusion, permeability, and inflammation in kidney. Improvement of this endothelial dysfunction could be a good approach to treating ischemia-reperfusion-induced renal injury. Cartilage oligomeric matrix protein-angiopoietin-1 (COMP-Ang1) is a variant of native angiogenic factor angiopoietin-1 engineered to have higher activity. We evaluated the protective effect of COMP-Ang1 in an ischemia-reperfusion renal injury model. COMP-Ang1 preserved renal peritubular capillaries after ischemia-reperfusion injury without recruiting pericytes. Pretreatment with COMP-Ang1 attenuated the increase of blood urea nitrogen and serum creatinine levels after ischemia-reperfusion. In addition, the morphological examination indicated less tubular injury in mice pretreated with COMP-Ang1 than in those treated with the vehicle. COMP-Ang1 treatment reduced the increase in the number of Gr-1-positive neutrophils or ER-HR3-positive macrophages infiltrating kidneys, increased phosphorylation of Akt, and preserved renal tissue perfusion flow and microvascular permeability. Furthermore, COMP-Ang1 decreased renal interstitial fibrosis 30 days after the ischemia-reperfusion injury. In conclusion, COMP-Ang1 can be a possible endothelial cell-targeted therapy for preventing ischemia-reperfusion-induced acute kidney injury.

ischemia-reperfusion-injured kidney; endothelial cells; cartilage oligomeric matrix protein-angiopoietin-1