Abstract
Reactive oxygen species (ROS) play an important role in the process of cardiovascular degeneration. We evaluated the potential of a controlled, local induction of ROS-release by application of rose bengal (RB) and photo energy to induce atherosclerosis-like focal vascular degeneration in vivo. After injection of RB, rats fed with a pro-degenerative diet underwent focal irradiation of the abdominal aorta by a green laser (ROS group), while the controls received irradiation without RB. Aortic tissue was analyzed by histology and immunohistochemistry at 0, 2, 4, 8, 28 and 56 days (n = 5). The intimal surface topography was analyzed by scanning electron microscopy. In the ROS group, an initial thrombus formation had disappeared by day 8. Similarly, ROS-derived products displayed the highest concentrations at day 0. Relative matrix metalloproteinase (MMP) activity achieved a maximum after 8 days (ROS group vs. control group: 1.60 ± 0.11 vs. 0.98 ± 0.01; p < 0.001). After 28 days, no significant differences in any aspect were found between the ROS group and the controls. However, after 56 days, the aortic tissue of ROS animals exhibited relative media-pronounced thickening (ROS vs. control: 2.15 ± 0.19 vs. 0.87 ± 0.10; p < 0.001) with focal calcification and reduced expression of alpha smooth muscle actin (aSMA). The ROS-releasing application of RB and photo energy allowed for the induction of vascular degeneration in a rodent model. This protocol may be used for the focal induction of vascular disease without systemic side effects and can thereby elucidate the role of ROS in the multifactorial processes of vessel degeneration and atherogenesis.
Highlights
A growing body of evidence supports the theory that reactive oxygen species (ROS) are a causative component in the pathophysiology of degenerative cardiovascular diseases, such as arterial hypertension [1], thrombosis [2] and atherosclerosis [3]
Calcium serum levels were significantly higher in the diet-exposed groups at early time points, but this statistically significant difference was lost at the late time point of t = 56 d (Fig 1A)
standard errors of the mean (SEM) analysis of the aortic wall topography displayed in the ROS group a focal thrombus at t = 0 at the region of irradiation (Fig 2A; arrow)
Summary
A growing body of evidence supports the theory that reactive oxygen species (ROS) are a causative component in the pathophysiology of degenerative cardiovascular diseases, such as arterial hypertension [1], thrombosis [2] and atherosclerosis [3]. Within the complex pathways of atherosclerosis, the discussed interactions of ROS are numerous. Oxidative stress impairs endothelial function, enhances smooth muscle cell (SMC) proliferation and inflammation and foam cell genesis by low-density lipoprotein (LDL) oxidation [4]. Vascular calcification can be promoted by oxidative stress-induced osteogenic transcription factors [5].
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