Project OUR Scholar project: Mechanotransduction of nuclear metabolic signaling in progerin-expressing endothelial cells Program Engineering Term Academic Year 2025 Status Accepted Research Area biomedical engineering, cell mechanics, live cell imaging Description The human aging process increases the risk of cancer and cardiovascular diseases that together account for the most common causes of death in United States. Nuclear lamina, a network of intermediate filaments located right underneath the nuclear envelope, is implicated in the aging process. It plays a critical role in the structural integrity of the nucleus as well as in connecting with cell cytoskeleton. A mutant truncated form of lamin called progerin is responsible for premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). AMP-activated protein kinase (AMPK) is a crucial regulator of cellular energy homeostasis, significantly influencing aging by modulating metabolic pathways. In this project, we will use fluorescence resonance energy transfer (FRET) imaging and visualize the activity of AMPK signaling in the nucleus, mitochondria, and cytoplasm in progerin-expressing endothelial cells under flow-induced shear stress. Supervisor Sungsoo Na Mentor Sungsoo Na Type of work required OUR Scholars will be involved in a range of techniques essential for studying cell mechanics and live cell imaging. This includes cell culture, transfection (introducing plasmids into cells), advanced live cell imaging using the FRET technique, and image analysis and quantification of cell signaling activity. Websites https://engineering.purdue.edu/BME/People/ptProfile?resource_id=299025 Qualifications At least 3.0 GPA. Knowledge of cell culture is recommended. Credit Hours 0 Weekly Hours 10 (estimated)