The mannose-binding lectin pathway is a significant contributor to reperfusion injury in the type 2 diabetic heart

Laura R. La Bonte, Betsy Dokken, Grace Davis-Gorman, Gregory L. Stahl, Paul F. McDonagh

Research output: Contribution to journalArticle

19 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)172-180
Number of pages9
JournalDiabetes and Vascular Disease Research
Volume6
Issue number3
DOIs
StatePublished - Jul 2009

Keywords

  • Complement
  • Inflammation
  • Ischaemia-reperfusion injury
  • Zucker diabetic fatty rat

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Cardiology and Cardiovascular Medicine

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