Speaker
Hanjoong Jo Ph.D.
Date
Location
University of Houston
Abstract
Atherosclerosis is the major underlying cause of myocardial infarction and stroke. It occurs preferentially in arterial regions exposed to disturbed flow (d-flow) by mechanisms involving broad changes in the expression of genes. Using the partial carotid ligation model of atherosclerosis in mice and single-cell OMICs studies, we revealed the roles of flow-sensitive genes in endothelial dysfunction and atherosclerosis. The single-cell OMICs and validation studies revealed that d-flow reprograms endothelial cells to proatherogenic phenotypes, including inflammation, endothelial-to-mesenchymal transition (End-MT), and endothelial-to-immune cell-like transition (EndIT). The scRNAseq study revealed several novel flow-sensitive genes, such as HEG1, and how they regulate endothelial function and atherosclerosis. I will also discuss how we target those flow-sensitive genes to develop novel anti-atherogenic therapeutics and pursue endothelial-targeted delivery of therapeutics.