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Cardiac Repair/Remodeling Following Infarction in Mice with Targeted Deletion of NADPH Oxidase
Author(s) -
Zhao Wenyuan,
Yan Ran,
Zhao Dan,
Chen Yuanjian,
Sun Yao
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.21.5.a130-c
Subject(s) - nadph oxidase , myocyte , myocardial infarction , ventricular remodeling , knockout mouse , myofibroblast , medicine , apoptosis , reactive oxygen species , oxidative stress , endocrinology , chemistry , cardiology , biology , microbiology and biotechnology , fibrosis , biochemistry , receptor
Oxidative stress has been demonstrated to involve in progression of heart failure. NADPH oxidases are a major source of reactive oxygen species in the heart. Herein, we studied left ventricular repair/remodeling after myocardial infarction (MI) in mice and the involvement of NADPH oxidase on the process. Wild‐type C57BL/6J mice and NADPH oxidase subunit (gp91phox) knockout mice were subjected to MI by ligation of the left coronary artery. At day 3, 7, 14, and 28 postMI (n=10/group/time point), we addressed: cardiac gp91phox gene expression, infarct size, myocyte apoptosis, cells involving cardiac repair, type 1 collagen gene expression and collagen volume. In wild type mice and compared to sham‐operated animals, we observed significantly increased gp91phox expression in the infarcted myocardium particularly in the early stage of MI, abundant apoptotic myocytes primarily at border zones at day 3 and 7, accumulated ED‐1+ macrophages and ‐smooth muscle actin+ myofibroblasts at infarct site, significantly increased type 1 collagen gene expression peaked at day 7 and continuously increased collagen volume in the infarcted myocardium for over the course of 4 wks. In gp91phox knockout mice, we found significantly reduced apoptotic myocytes at the border zones at day 7. However, infarct size, inflammatory/fibrogenic responses were not influenced by the genotype. Thus, targeted deletion of the NADPH subunit gp91phox suppresses myocyte apoptosis, but does not affect cardiac repair/remodeling following MI.