%0 Journal Article
%T Fibrous Cap Smooth Muscle Cells in Atherosclerotic Coronary Arteries Do Not Express Pluripotent Stem Cell Markers
%A Melanie Sullivan
%A Anthony Zulli
%J Journal of Angiology
%D 2013
%R 10.1155/2013/592815
%X Rupture of the coronary artery fibrous cap is a common cause of myocardial infarction, and bone marrow derived cells could play a role in preventing plaque rupture. It is currently unknown whether smooth muscle cells within coronary artery fibrous cap formation are of mature phenotype. Objective. To characterize cells expressing bone marrow stem cells of embryonic type (ESC) markers in coronary artery fibrous cap formation. Design. New Zealand White rabbits were fed a diet supplemented with 0.5% cholesterol£¿£¿+£¿£¿1% methionine£¿£¿+£¿£¿5% peanut oil for 4 weeks and then a normal diet for 9 weeks. The left main coronary artery was excised from the heart, processed for paraffin and immunohistochemistry was performed by standard techniques. Results. Oct-4, SSEA 1, 3, and 4 were all present within in atherosclerotic plaque core, codistributed with RAM-11, and were sparingly found in the fibrous cap, but TRA-1-60 and TRA-1-81 positive cells were scarce. Core but not fibrous cap smooth muscle (SMC actin+) cells also showed codistribution with ESC markers. Conclusions. These results suggest that smooth muscle cells present in the fibrous cap do not express ESC markers, indicative of a mature cell. 1. Introduction Rupture of coronary artery fibrous cap is a major cause of myocardial infarct [1]. Inhibition of the HMG CoA reductase enzyme and renin angiotensin system have been one of the most successful therapies in reducing this burden, possibly by increasing the formation of a stable fibrous cap. Interestingly, stem cells can be regulated by the same pharmacological therapy, providing a possible explanation as to the beneficial effects of treatments [2]. For example, simvastatin has been shown to normalise endothelial progenitor cells in obese patients to those observed in nonobese controls [3] and angiotensin II receptor blockers increased endothelial progenitor cells in diabetic patients [4], and modulation of these types of cells is also observed with angiotensin converting enzyme inhibitors [5]. Thus, the characterization of stem cell populations in coronary artery disease will aid in understanding whether standard pharmacological treatments can affect the population of such undifferentiated cells. Recent studies have suggested that the origin of smooth muscle cells in atherosclerotic fibrous caps might not be from the circulation [6] as had been enthusiastically embraced but derive from the local medial SMC layer [7, 8]. Thus, in this study, it was hypothesised that if smooth muscle cells originated from the circulation and were of primitive type, then the cells
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