Heart disease is a major cause of death in the Western world. In the past three decades there has been a number of improvements in artificial devices and surgical techniques for cardiovascular disease; however, there is still a need for novel devices, especially for those individuals who cannot receive conventional therapy. The major disadvantage of current artificial devices lies in the fact that they cannot grow, remodel, or repair in vivo. Tissue engineering offers the possibility of developing a biological substitute material in vitro with the inherent mechanical, chemical, biological, and morphological properties required in vivo, on an individual patient basis. In order to develop a true biological cardiovascular device a dynamic physiological environment needs to be created. One approach that employs the use of a simulated biological environment is a bioreactor in which the in vivo biomechanical and biochemical conditions are created in vitro for functional tissue development. A review of the current state of the art bioreactors for the generation of tissue engineered cardiovascular devices is presented in this study. The effect of the simulated physiological environment of the bioreactor on tissue development is examined with respect to the materials properties of vascular grafts, heart valves, and cardiac muscles developed in these bioreactors.
Percutaneous stent implantation has revolutionized the clinical treatment of occluded arteries. Nevertheless, there is still a large unmet need to prevent re-occlusion after implantation. Consequently, a niche exists for a cost-effective pre-clinical method of evaluating novel interventional devices in human models. Therefore, the development of a coronary model artery offers tremendous potential for the treatment of endothelial cell dysfunction and restenosis. As a first step, we employ tissue-engineering principles to examine the effect of stent deployment upon endothelial cells in a tubular in vitro system capable of replicating the coronary artery biomechanical environment. In particular, the cellular and molecular changes pertaining to inflammation, proliferation, and death were assessed after stent deployment. Real-time quantitative PCR demonstrated increased expression of genes encoding for E-Selectin, ICAM-1, and VCAM-1; markers associated with an inflammatory response in vivo. Further, an increase in the pro-apoptotic protein Bax was paralleled with a decrease in the anti-apoptotic protein Bcl-2; however, apoptotic morphology was not observed. Interestingly, transcription of c-fos increased, whereas Ki67 levels fell over the same period. One hypothesis is that these results are in response to the altered local hemodynamic environment induced by stent deployment. Most significantly, this study highlights the potential of a biomimetic hemodynamic bioreactor combined with a gene expression analysis to evaluate, with greater specificity, the performance and interaction of stents with the endothelial layer in a controlled environment.
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