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Renal Ischemia/Reperfusion Injury: Functional Tissue Preservation by Anti-Activated 1 Integrin Therapy

Ana Molina^*, María Ubeda^*, María M. Escribese^*, Laura García-Bermejo^*, David Sancho, GuillermoPé de Lema , Fernando Liaño, Carlos Cabañas^||, Francisco Sánchez-Madrid and Francisco Mampaso^*

^* Department of Pathology, Hospital Ramón y Cajal, Universidad de Alcalá, Madrid, Spain; Department of Immunology, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; Medizinische Poliklinic der Ludwig Maximillians-Universitat, Munich, Germany; Department of Nephrology, Hospital Ramón y Cajal, Universidad de Alcalá, Madrid, Spain; and ^|| Institute of Pharmacology and Toxicology (Centro Mixto CSIC-UCM), Facultad de Medicina, Universidad Complutense, Madrid, Spain

Address correspondence to: Dr. Francisco Mampaso, Hospital Ramón y Cajal, Departamento de Patología, Carretera de Colmenar, Km 9.1, 28034 Madrid, Spain. Phone: 34-91-3368052; Fax: 34-91-3369016; E-mail: fmampaso.hrc{at}salud.madrid.org

Renal ischemia/reperfusion injury (IRI) is an important cause of acute renal failure. Cellular and molecular responses of the kidney to IRI are complex and not fully understood. 1 integrins localize to the basal surface of tubular epithelium interacting with extracellular matrix components of the basal membrane, including collagen IV. Whether preservation of tubular epithelium integrity could be a therapeutic approach for IRI was assessed. The effects of HUTS-21 mAb administration, which recognizes an activation-dependent epitope of 1 integrins, in a rat model of IRI were investigated. Preischemic HUTS-21 administration resulted in the preservation of renal functional and histopathologic parameters. Analyses of activated 1 integrins expression and focal adhesion kinase phosphorylation suggest that its deactivation after IRI was prevented by HUTS-21 treatment. Moreover, HUTS-21 impaired the inflammatory response in vivo, as indicated by inhibition of proinflammatory mediators and the absence of infiltrating cells. Ex vivo adhesion assays using reperfused kidneys revealed that HUTS-21 induced a significant increase of epithelial cell attachment to collagen IV. In conclusion, the data provide evidence that HUTS-21 has a protective effect in renal IRI, preventing tubular epithelial cell detachment by preserving activated 1 integrins functions.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673