In the past 20 years, two new mechanisms of hypertension have been defined: one is oxidative injury and the second is inflammation. Our lab has shown that dendritic cells (DCs) from hypertensive mice accumulate isolevuglandins that adduct to proteins and promote T cell activation. In hypertension, the endothelium is activated to produce reactive oxygen species and to express adhesion molecules and chemokines that attract inflammatory cells. In my project, we hypothesized that human endothelial cells exposed to mechanical stretch will promote conversion of human monocytes into activated DCs. Therefore, I study this conversion when monocytes co-cultured with human aortic endothelial cells exposed to either normal cyclical stretch (5%) or hypertensive cyclical stretch (10%) using the Flexcell® Tension System. I also study the different signaling molecules that could potentially be facilitating this process in hopes of understanding the mechanism of action.
Graduate Student, Harrison laboratory, Molecular Physiology & Biophysics