Speaker
Professor Renita Horton
Date
Location
SEC 204
Abstract
Traditional in vitro studies poorly recapitulate properties of the native in vivo microenvironment. Creating in vitro systems capable of mimicking features such as tissue architecture, shear, and cell-cell interactions may prove beneficial in studying disease mechanisms and identifying novel therapeutics. Further, these models can serve as testbeds for drug efficacy and toxicity assays. We seek to build physiologically relevant models to investigate cardiac-related disease mechanisms.
We previously designed a cardiac dysfunction model using engineered cardiac tissues and angiotensin II (ANG II), a peptide involved in cardiac remodeling, growth, and apoptosis. Dysregulation of ANG II has been associated with hypertension, hypertrophy, and heart failure. We questioned whether exposing engineered cardiac tissues to ANG II would induce disease features in our model. We found that ANG II exposure led to functional decline in the engineered tissues evident by depressed contractile stress generation and elevated early after depolarization events. ANG II tissues also exhibited the reactivation of fetal related genes. The goal of this study was to demonstrate that our system could effectively recapitulate features of cardiac dysfunction by testing the effects of ANG II on the structure, function and pathological remodeling of engineered cardiac tissues. We are now expanding our focus to investigate the effect of chronic diseases on heart health.
We previously designed a cardiac dysfunction model using engineered cardiac tissues and angiotensin II (ANG II), a peptide involved in cardiac remodeling, growth, and apoptosis. Dysregulation of ANG II has been associated with hypertension, hypertrophy, and heart failure. We questioned whether exposing engineered cardiac tissues to ANG II would induce disease features in our model. We found that ANG II exposure led to functional decline in the engineered tissues evident by depressed contractile stress generation and elevated early after depolarization events. ANG II tissues also exhibited the reactivation of fetal related genes. The goal of this study was to demonstrate that our system could effectively recapitulate features of cardiac dysfunction by testing the effects of ANG II on the structure, function and pathological remodeling of engineered cardiac tissues. We are now expanding our focus to investigate the effect of chronic diseases on heart health.