|Aguilar, Victor||Atherosclerotic plaque growth is subject to factors beyond an individual’s diet. Growth is subject to factors such as blood flow hemodynamics, inflammation signals, and cell-cell interactions. My objective is to understand how these factors affect vascularization. Prior research has shown that vascular growth is enhanced by the presence of oxidized lipids, a phenomenon that was shown to be dependent on lipid uptake protein CD36. I am interested in utilizing CD36 expression to analyze changes in angiogenic gene expression and cell signaling in endothelium exposed to pro-atherogenic conditions in vitro. This work will incorporate in vivo work on transgenic endothelial-specific CD36-null mice to assess impact on long-term progression of induced atherosclerosis.||Irena Levitan, Ph.D. and Richard Minshall, Ph.D.||email@example.com|
|Sargis, Timothy||When activated by its ligand Dll4, Notch1 signaling acts as a negative regulator of angiogenic sprout initiation. Conversely, the Notch ligand Jagged1 has been discovered to be pro-angiogenic. Endothelial-specific Jagged1 loss leads to reduced angiogenesis during retinal development, wound healing, and tumor angiogenesis. How Jagged1 mediates its pro-angiogenic function is currently not well understood. Several models for Jagged1 function have been proposed: Jagged1 may be a competitor of Dll4, or a unique Notch signal activator. We hypothesize that Jagged1 interacts with another Notch protein, Notch4, to promote angiogenesis and that this signaling is distinct from the role of Dll4/Notch1 signaling. This project aims to describe a new signaling pair (Jagged1-Notch4) and to develop new approaches to promote wound healing through regulation of Jagged1 or Notch4 activities.||Jan Kitajewski, Ph.D. and Luisa DiPietro, DDS, Ph.D.||firstname.lastname@example.org|
The VBST-TP is funded by training grant (T32 HL144459) from the National, Heart, Lung, and Blood Institute (NHLBI).