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Journals The FASEB Journal Volume 19 Issue 14

Transgenic activation of the kallikrein-kinin system inhibits intramyocardial inflammation, endothelial dysfunction and oxidative stress in experimental diabetic cardiomyopathy Carsten Tschöpe 1 , Thomas Walther, Felicitas Escher, Frank Spillmann, Jing Du, Christine Altmann * , Ingolf Schimke † , Michael Bader ‡ , Carlos F. Sanchez-Ferrer, Heinz-Peter Schultheiss and Michel Noutsias Department of Cardiology and Pneumonology, Charité-University Medicine Berlin, Campus Benjamin Franklin and * Campus Mitte, Germany; † Max-Delbrück-Center for Molecular Medicine, Berlin, Germany; and ‡ Department of Pharmacology and Therapeutics, Faculty of Medicine, Autonomous University of Madrid, Spain 1 Correspondence: Department of Cardiology and Pneumology, Charité-University Medicine Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, D-12220 Berlin, Germany. E-Mail: ctschoepe@yahoo.com <h3>SPECIFIC AIMS</h3> In light of the possible involvement of intramyocardial inflammation in diabetic cardiomyopathy, we investigated cardiac CAMs expression (ICAM-1 and VCAM-1) and β 2 -leukocyte integrins <h3>+</h3> infiltrates as well as cytokine (TNFα and IL-1β) expression in STZ-induced diabetic wild type rats as well as the role of the cardioprotective role of the kallikein-kinin system (KKS) under this hyperglycemic condition by investigating transgenic diabetic rats harboring the human kallikrein 1 gene TGR(hKLK1). We also assessed endothelial function by measuring vascular tone in isolated mesenteric microvessels, and the degree of

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Transgenic activation of the kallikrein-kinin system inhibits intramyocardial inflammation, endothelial dysfunction and oxidative stress in experimental diabetic cardiomyopathy

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