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

doi:10.1177/1479164109336051

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

Medicine

Research output: Contribution to journal › Article › peer-review

20 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 language	English (US)
Pages (from-to)	172-180
Number of pages	9
Journal	Diabetes and Vascular Disease Research
Volume	6
Issue number	3
DOIs	https://doi.org/10.1177/1479164109336051
State	Published - 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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10.1177/1479164109336051

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

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.",

keywords = "Complement, Inflammation, Ischaemia-reperfusion injury, Zucker diabetic fatty rat",

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AU - Dokken, Betsy

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AU - Stahl, Gregory L.

AU - McDonagh, Paul F.

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N2 - 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.

AB - 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.

KW - Complement

KW - Inflammation

KW - Ischaemia-reperfusion injury

KW - Zucker diabetic fatty rat

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

Abstract

Keywords

ASJC Scopus subject areas

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