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Permanent link (DOI): https://doi.org/10.7939/R3P62W

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The role of cytochrome P450 and the protective effect of EETs against isoproterenol-induced cellular hypertrophy in rat H9c2 cell line Open Access

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Other title
Subject/Keyword
hypertrophy
H9c2 cell
cytochrome P450
EETs
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Tse, Mandy M.Y.
Supervisor and department
Ayman, El-Kadi (Pharmacy and Pharmaceutical Sciences)
Examining committee member and department
Lars-Oliver, Klotz (Pharmacy and Pharmaceutical Sciences)
Paul, Jurasz (Pharmacy and Pharmaceutical Sciences)
Glen, Baker (Psychiatry)
Department
Faculty of Pharmacy and Pharmaceutical Sciences
Specialization
Pharmaceutical Sciences
Date accepted
2013-01-05T06:46:43Z
Graduation date
2013-06
Degree
Master of Science
Degree level
Master's
Abstract
Cytochrome P450 (CYP) enzymes have been identified in the heart and their levels have been reported to be altered during cardiac hypertrophy and heart failure. Furthermore, CYP enzymes have been shown to metabolize arachidonic acid to cardioprotective epoxyeicosatrienoic acids (EETs) and cardiotoxic 20-hydroxyeicosatetraenoic acid (20-HETE). Therefore, the objective of this study was to investigate the protective effect of EETs and the role of CYPs and soluble epoxide hydrolase (sEH) in the development of cardiac hypertrophy. Our results showed that isoproterenol-induced cellular hypertrophy caused a significant induction in the mRNA expression of CYP1A1, CYP1B1, CYP2J3, CYP4F4, CYP4F5 and EPHX2 in H9c2 cells. Also, we demonstrated that 11,12- and 14,15-EETs significantly attenuated the isoproterenol-mediated induction of hypertrophic markers, ANP and BNP, as well as CYP1A1, CYP2J3, CYP4F4, CYP4F5 and EPHX2. Furthermore, we showed that the inhibition of sEH by TUPS significantly decreased the isoproterenol-mediated induction of ANP, BNP, CYP1A1, CYP2J3, CYP4F4, CYP4F5 and EPHX2.
Language
English
DOI
doi:10.7939/R3P62W
Rights
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 these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before 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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