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Tumor necrosis factor triggers the expression and activation of matrix metalloproteinases through NADPH-dependent superoxide production Open Access


Other title
pressure overload cardiac disease
matrix metalloproteinases
reactive oxygen species
reactive nitrogen species
neonatal cardiomyocytes and cardiofibroblasts isolation
tumor necrosis factor
Type of item
Degree grantor
University of Alberta
Author or creator
Awad, Ahmed
Supervisor and department
Examining committee member and department
Schulz, Richard (Pediatrics adn Pharmacology)
Kassiri, Zamaneh (Physiology)
Davidge, Sandara (Obstetrics/Gynecology and Physiology)
Jahroudi, Nadia (Medicine)
Department of Physiology

Date accepted
Graduation date
Master of Science
Degree level
Tumor necrosis factor (TNF) is upregulated in a number of cardiomyopathies. This thesis investigates TNF in triggering the expression and activation of matrix metalloproteinases (MMPs) in pressure overload cardiac disease, and explores the role of superoxide. Cardiac pressure overload was generated in adult wild-type and TNF-/- mice by transverse aortic constriction. Isolated cardiomyocytes and cardiofibroblasts from neonatal mice ventricles were treated with recombinant TNF (rTNF), and MMP induction and activation were assessed, with and without apocynin (a NADPH-oxidase inhibitor). TNF-/- mice showed less superoxide production and MMP activation, compared to wild-type mice, following pressure overload. rTNF upregulated the production of NADPH-dependent superoxide in cardiomyocytes as early as 1 hour (24 hours in cardiofibroblasts). rTNF also increased the expression of MMP-9 and MMP-12 in cardiomyocytes more than in cardiofibroblasts, and MMP-8 and MMP-13 more in cardiofibroblasts. This induction in both cardiac cell types was concomitant with superoxide production.
License granted by Ahmed Awad ( on 2010-01-28T20:37:33Z (GMT): Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of the above terms. The author reserves all other publication and other rights in association with the copyright in the thesis, and except as herein provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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File title: Dedication
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