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Reactive Oxygen Species Promote Angiogenesis in the Infarcted Rat Heart
Author(s) -
Zhao Wenyuan,
Zhao Tiqiang,
Chen Yuanjian,
Sun Yao
Publication year - 2009
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.23.1_supplement.576.1
Subject(s) - angiogenesis , apocynin , reactive oxygen species , nadph oxidase , myocardial infarction , medicine , cardiology , oxidative stress , endocrinology , chemistry , biochemistry
Cardiac reactive oxygen species (ROS) production is significantly increased following infarction (MI), particularly at early stage. Herein we sought to determine whether ROS play a role on angiogenesis in the infarcted heart. Experimental MI rats were treated with combined antioxidants, tempol and apocynin, each 120mg/kg/day. Non‐treated MI rats served as controls. Hearts were collected at day 1, 3, 7, 14, 28 and 42. We examined effect of antioxidants on angiogenesis in the infarcted myocardium. Following MI, NADPH oxidase (gp91phox subunit) was significantly increased in the infarcted myocardium at day 3, reached peak at day 7, and gradually declined thereafter. In the infarcted region, existing vessels were lost at day 1 postMI. Newly formed vessels appeared in the border zone as early as day 3, followed by the infarcted myocardium. Vascular density peaked at day 7 and 14, and progressively reduced thereafter. Antioxidants significantly reduced cardiac vascular density at day 7 and 14, but not in the later time points. Thus, angiogenesis is activated in the infarcted myocardium in the first two weeks and becomes quiescent in the late stage of MI, which is temporally and spatially coincident with increased ROS production. Our study also indicates that ROS promote angiogenesis in the infarcted myocardium. Further studies are required to determine the mechanisms responsible for ROS mediated cardiac angiogenesis.