Hutchinson-Gilford progeria syndrome (HGPS) is a rare, genetic disorder caused by a mutation in LMNA gene that results in a mutant lamin A protein product known as progerin. Children with the disease suffer from accelerated organ degeneration, and death results almost exclusively from coronary artery diseases or strokes at an average age of 14.6 years. Endothelial dysfunction is a key contributor to the cardiovascular pathobiology as the endothelium maintains vascular homeostasis and vascular tone by activating endothelial nitric oxide synthase (eNOS) that responsible for nitric oxide (NO) production. Despite the vast knowledge of endothelial dysfunction in the pathogenesis of cardiovascular disease, very little known about the role of progerin in the disruption of endothelial function. Thus, to address how progerin disrupt endothelial function in HGPS, we proposed two specific aims: (i) characterize human induced pluripotent stem cell (iPSC)-derived normal and HGPS vascular endothelial cells; (ii) examine the underlying mechanisms of progerin-induced endothelial dysfunction under static and fluidic culture conditions. To this end, this project entails the development of bioreactors capable of applying low fluid shear stresses on the seeded cells.