Abstract | BACKGROUND: METHODS AND RESULTS: gp91( phox) knockout (KO) and wild-type (WT) animals underwent coronary artery ligation. Mortality was significant higher in the gp91( phox) KO mice. However, transthoracic echocardiography performed at days 1, 7, and 56 at mid-papillary levels revealed that progression of left ventricular remodeling was not influenced by the genotype. Moreover, systemic oxidative stress was not reduced in gp91( phox) KO mice as indicated by a significant increase in lipid peroxides potentially mediated by an increase of the NADPH subunit nox-1 in gp91( phox) KO mice. CONCLUSION: Targeted deletion of the NADPH subunit gp91( phox) does not affect left ventricular remodeling following myocardial infarction and does not decrease the production of oxidative stress. However, the final role of the different NADPH subunits in the heart under pathophysiologic conditions remains to be determined.
|
Authors | Stefan Frantz, Ralf P Brandes, Kai Hu, Konrad Rammelt, Jürgen Wolf, Heidi Scheuermann, Georg Ertl, Johann Bauersachs |
Journal | Basic research in cardiology
(Basic Res Cardiol)
Vol. 101
Issue 2
Pg. 127-32
(Mar 2006)
ISSN: 0300-8428 [Print] Germany |
PMID | 16273323
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
Chemical References |
- Membrane Glycoproteins
- Cybb protein, mouse
- NADPH Oxidase 2
- NADPH Oxidases
|
Topics |
- Animals
- Echocardiography
- Gene Deletion
- Membrane Glycoproteins
(genetics)
- Mice
- Mice, Knockout
- Myocardial Infarction
(physiopathology)
- NADPH Oxidase 2
- NADPH Oxidases
(genetics)
- Oxidative Stress
(physiology)
- Ventricular Remodeling
(genetics)
|