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Complement Deposition is Increased in the Type 2 Diabetic Heart Following Ischemia/Reperfusion
Author(s) -
La Bonte Laura,
DavisGorman Grace,
Stahl Gregory L.,
McDonagh Paul F.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1225-b
Subject(s) - medicine , ischemia , cardiology , diabetes mellitus , complement system , inflammation , type 2 diabetes , complement (music) , endocrinology , antibody , immunology , biochemistry , chemistry , phenotype , complementation , gene
A relationship exists between chronic inflammation and the cardiovascular complications of diabetes, but exactly how inflammation exacerbates ischemic heart disease is not clear. Complement activation plays an important role in the inflammatory response and is known to be involved in ischemia/reperfusion (I/R) injury in the non‐diabetic heart. The purpose of this study was to determine if complement deposition is enhanced in the type 2 diabetic heart following ischemia. Non‐diabetic Zucker Lean Control (ZLC) and Zucker Diabetic Fatty (ZDF) rats underwent left anterior descending (LAD) coronary artery occlusion for 30 minutes followed by 120 minutes of reperfusion. At the end of reperfusion, cardiac tissue samples were freeze‐fixed, sectioned, and stained for complement deposition using an HRP‐conjugated anti‐C3 antibody. We found that there is significantly greater complement deposition in the area‐at‐risk of the ZDF compared to the ZLC (ZLC: 44.3 ± 8.5%; ZDF: 82.4 ± 12.5%; p < 0.05). These findings parallel infarct size measurements in which the infarct‐to‐AAR percentage of the ZDF is significantly greater than control (ZLC: 25.7% I/AAR; ZDF: 56.9% I/AAR; p < 0.05 using Kruskal‐Wallis ANOVA). These findings indicate that increased complement deposition in the at‐risk region following I/R injury is associated with an exacerbated inflammatory response and may therefore contribute to the increased tissue injury observed in the type 2 diabetic heart. Supported by NIH HLB 58859 and AHA 0610018Z.