UC Irvine

The reduction of blood flow, or ischemia, compromises the contractile function of the heart by damaging cardiomyocytes. Macrophages from the immune system play a key role during cardiac repair to preserve the heart physical integrity (i.e preventing leaks) as well as potentially acting to preserve some of the function. Therefore, studying the interaction between cardiomyocytes and macrophages would help to better understand the underlying mechanisms of cardiac repair. However, co-culture of cardiomyocytes and macrophages has not been extensively studied due to technical challenges. The first part of this thesis work aimed to explore whether macrophage culture media components affect cardiomyocyte health during in vitro culture. As part of this, the effects of media components on cellular health were investigated by observing cell size and morphology changes. It was observed that different media compositions altered cell size and morphology, suggesting that macrophages and/or macrophage-induced factors had a negative impact on healthy cardiomyocytes. An ischemia model was tested in the second part of this study. The effectiveness of an inexpensive and easy-to-implement model was tested to introduce hypoxia on cardiac fibroblasts and cardiomyocytes. The results showed that there was no significant reduction in both primary cardiac fibroblasts and neonatal cardiomyocytes population, suggesting that the model failed to establish hypoxia during the time period studied. Although the model was unsuccessful, this research provided preliminary data for creating simple ischemic devices.