| Summary: | 碩士 === 國立交通大學 === 材料科學與工程學系奈米科技碩博士班 === 101 === Topography was been reported to infuence the cells' behavior. However, it is very challenging to know long term biological effects from each individual contributing factor such as biocompatibility, inflammatory and apoptosis. Nitric oxide (NO) is a highly reactive nitrogen radical implicated in inflammatory responses. We investigated the signaling pathway involved in inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOs) in cultured cardiomyoblast H9c2 . Here we propose that the surface topology in contact with the living cells could be designed to control apoptosis and inflammation level such cells. The cardiomyoblast H9c2 was cultured on nanodot arrays with dot diameters ranging between 10 and 200 nm. In the present study, fluctuation of NO production is modulated by nanodot arrays in H9c2 with 1, 3, 5, 7, 14 days culture. With time course, the cell NO level in H9c2 increased with 100 to 200 nm nanodot arrays compared to the flat surface. A similar trend of eNOs signal gene expression was observed in H9c2. We also confirm of the topological control of eNOs pathway. Immunostaining indicated that nanodots lager than 50-nm induced cell eNOs expression.
This suggests that nanodots of 100- and 200-nm triggered inflammatory stress response (NO level). In summary, nanotopography controls cell apoptosis and inflammatory responses. By adjusting the nanodot diameter, we could modulate the inflammatory response and expression of function-related genes and proteins in the cardiovascular cell system. The nanotopography mediated control of cell inflammatory and appotosis provides potential insight for designing cardiovascular implants.
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