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Originally published online as doi:10.2353/ajpath.2007.070184 on November 30, 2007

Published online before print November 30, 2007
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(American Journal of Pathology. 2007;171:1743-1752.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.070184

Myeloperoxidase Is Critically Involved in the Induction of Organ Damage after Renal Ischemia Reperfusion

Robert A. Matthijsen*, Dennis Huugen{dagger}, Nicole T. Hoebers*, Bart de Vries*, Carine J. Peutz-Kootstra{ddagger}, Yasuaki Aratani§, Mohamed R. Daha, Jan Willem Cohen Tervaert{dagger}, Wim A. Buurman* and Peter Heeringa{dagger}

From the Department of General Surgery, * Nutrition, and Toxicology, Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands; the Departments of Immunology{dagger} and Pathology,{ddagger} Cardiovascular Research Institute Maastricht, Academic Hospital Maastricht, Maastricht, The Netherlands; the Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands; and the Kihara Institute for Biological Research and Graduate School of Integrated Science,§ Yokohama City University, Yokohama, Japan

In this study the role of myeloperoxidase (MPO) in a murine (C57BL/6) model of ischemia and reperfusion (I/R)-induced renal failure was investigated. The renal function after I/R was analyzed in MPO-deficient (Mpo–/–) mice and compared with wild-type (WT) controls. A significant reduction in renal function loss (blood urea nitrogen) was observed after 24 hours of reperfusion of ischemically damaged kidneys in Mpo–/– mice compared with I/R WT controls (I/R Mpo–/– = 31.3 ± 1.7 mmol/L versus I/R WT = 42.8 ± 2.1 mmol/L, sham = 7.0 ± 0.5 mmol/L; P = 0.003). The early reperfusion phase (2 hours of reperfusion) was characterized by a substantial increase in apoptosis and early complement activation, surprisingly similar in Mpo–/– and WT mice. Improved renal function in Mpo–/– mice after extended reperfusion was accompanied by a reduced neutrophil influx (P = 0.017) compared with WT controls. Activation and deposition of complement was not significantly reduced in Mpo–/– mice compared with WT controls after 24 hours of reperfusion, indicating no specific in vivo role for MPO in activating complement after renal I/R. Taken together, these results demonstrated an important contribution of MPO in the induction of organ damage after renal I/R by influencing critical factors such as neutrophil extravasation but not complement activation.






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