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Published ahead of print on July 9, 2008
J Am Soc Nephrol 19: 1904-1918, 2008
© 2008 American Society of Nephrology
doi: 10.1681/ASN.2007111209
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BASIC RESEARCH

Macrophage Stimulating Protein May Promote Tubular Regeneration after Acute Injury

Vincenzo Cantaluppi*,{dagger}, Luigi Biancone*,{dagger}, Giuseppe Mauriello Romanazzi*, Federico Figliolini*, Silvia Beltramo*, Francesco Galimi{ddagger}, Maria Gavina Camboni{ddagger}, Elisa Deriu{ddagger}, Piergiulio Conaldi§, Antonella Bottelli||, Viviana Orlandi, Maria Beatriz Herrera*, Alfonso Pacitti{dagger}, Giuseppe Paolo Segoloni{dagger} and Giovanni Camussi*,{dagger}

* Research Center for Experimental Medicine and {dagger} Nephrology, Dialysis and Renal Transplantation Unit, Department of Internal Medicine, University of Torino, Torino, {ddagger} Department of Biomedical Sciences/National Institute of Biostructures and Biosystems (INBB), University of Sassari, Sassari, § Laboratory of Clinical Pathology, Microbiology and Virology, Mediterranean Institute for Transplantation and Advanced Specialized Therapies, University of Pittsburgh Medical Center, Palermo, and Departments of || Medicine/Public Health and Structural and Functional Biology, University of Insubria, Varese, Italy

Correspondence: Prof. G. Camussi, Cattedra di Nefrologia, Dipartimento di Medicina Interna, Ospedale Maggiore S. Giovanni Battista, Corso Dogliotti 14, 10126, Torino, Italy. Phone +39-011-6336708; Fax: +39-011-6631184; E-mail: giovanni.camussi{at}unito.it

Received for publication November 16, 2007. Accepted for publication April 16, 2008.

Macrophage-stimulating protein (MSP) exerts proliferative and antiapoptotic effects, suggesting that it may play a role in tubular regeneration after acute kidney injury. In this study, elevated plasma levels of MSP were found both in critically ill patients with acute renal failure and in recipients of renal allografts during the first week after transplantation. In addition, MSP and its receptor, RON, were markedly upregulated in the regenerative phase after glycerol-induced tubular injury in mice. In vitro, MSP stimulated tubular epithelial cell proliferation and conferred resistance to cisplatin-induced apoptosis by inhibiting caspase activation and modulating Fas, mitochondrial proteins, Akt, and extracellular signal–regulated kinase. MSP also enhanced migration, scattering, branching morphogenesis, tubulogenesis, and mesenchymal de-differentiation of surviving tubular cells. In addition, MSP induced an embryonic phenotype characterized by Pax-2 expression. In conclusion, MSP is upregulated during the regeneration of injured tubular cells, and it exerts multiple biologic effects that may aid recovery from acute kidney injury.






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