The Mannose-binding Lectin Pathway is a Significant Contributor to Reperfusion Injury in the Type 2 Diabetic Heart

Overview

Journal Diab Vasc Dis Res

Publisher Sage Publications

Specialty Cardiology & Vascular Diseases

Date 2010 Mar 11

PMID 20216929

Citations 15

Authors

Laura R La Bonte

Betsy Dokken

Grace Davis-Gorman

Gregory L Stahl

Paul F McDonagh

Affiliations

Soon will be listed here.

Abstract

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.

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