|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|
|Phillips, Evan, PhD||The objective of my project is to define and analyze cardiac lymphatic networks and the process of endogenous and growth factor-stimulated lymphangiogenesis in the context of cardiac hypertrophy. I am investigating the potential for cardiac lymphatic vessel generation, remodeling of the cardiac microenvironment, and immune cell trafficking via cardiac lymphatics. This project therefore requires an in situ morphological and molecular analysis method such as 3D multiplex microscopy. I will adapt tissue clearing appropriate for high-resolution 3D localization of multiple vascular, stromal, and inflammatory markers in cardiac tissue. This whole tissue imaging approach will help us understand the relevance of cardiac lymphatics in a new disease context and whether stimulated lymphangiogenesis hold therapeutic promise here.||Steve Seung-Young Lee, PhD and Jan Kitajewski, PhDemail@example.com|
The VBST-TP is funded by training grant (T32 HL144459) from the National, Heart, Lung, and Blood Institute (NHLBI).