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Diabetes and Vascular Disease Research
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The mannose-binding lectin pathway is a significant contributor to reperfusion injury in the type 2 diabetic heart

Laura R. La Bonte

Physiological Sciences Graduate Interdisciplinary Program, University of Arizona, USA, Sarver Heart Center, University of Arizona, USA

Betsy Dokken

Physiological Sciences Graduate Interdisciplinary Program, University of Arizona, USA, Sarver Heart Center, University of Arizona, USA

Grace Davis-Gorman

Department of Surgery, University of Arizona, USA, Sarver Heart Center, University of Arizona, USA

Gregory L. Stahl

Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, USA

Paul F. McDonagh

Physiological Sciences Graduate Interdisciplinary Program, University of Arizona, USA, Department of Surgery, University of Arizona, USA, Sarver Heart Center, University of Arizona, USA, pmcdonag{at}email.arizona.edu

The severity of ischaemic heart disease is markedly enhanced in type 2 diabetes.We recently reported that complement activation exacerbates I/R injury in the type 2 diabetic heart.The purpose of this study was to isolate and examine MBL pathway activation following I/R injury in the diabetic heart. ZLC and ZDF rats underwent 30 minutes of left coronary artery occlusion followed by 120 minutes of reperfusion.Two different groups of ZDF rats were treated with either FUT-175, a broad complement inhibitor, or P2D5, a monoclonal antibody raised against rat MBL-A. ZDF rats treated with FUT175 and P2D5 had significantly decreased myocardial infarct size, C3 deposition and neutrophil accumulation compared with untreated ZDF controls.Taken together, these findings indicate that the MBL pathway plays a key role in the severity of complement-mediated I/R injury in the type 2 diabetic heart.

Key Words: complement • Zucker Diabetic Fatty rat • inflammation • ischaemia-reperfusion injury

Diabetes and Vascular Disease Research, Vol. 6, No. 3, 172-180 (2009)
DOI: 10.1177/1479164109336051
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