Document Type
Research Poster
Publication Date
2014
Abstract
Angiogenesis is the sprouting of new blood vessels from pre-existing vessels initiated from vascular endothelial cells in response to exogenous chemical signals. Principle signals are vascular endothelial growth factors (VEGF) that direct cell growth and differentiation by binding to endothelial cell surface VEGF receptors (VEGFR). In Human Umbilical Vascular Endothelial Cells (HUVEC) initial sprouting cells or “tip cells” send signals to neighboring cells “stalk cells” responsible for sprout elongation. Multiple VEGF signals and receptors are known, but the main angiogenic signals are from VEGF-A through VEGFR-2 and VEGFR-3. Regulation of VEGF receptor expression can be influenced by the Notch signaling pathway that involves Delta Like Ligand 4 (Dll4) interaction with and its receptor, Notch-1, but also may be influenced by backtalk through a second Notch ligand, Jagged-1. We examined how Jagged-1 overexpression may affect VEGFR-2 and VEGFR-3 gene expression in HUVECs cells that are in “Tip Cell” mode vs. “Stalk Cell” mode. We found that overexpressing Jagged-1 in HUVECs that are not communicating through Notch increases VEGFR-2 and VEGFR-3 receptor expression but decrease these levels when cells can “talk” through Notch.
Recommended Citation
Stubbs, Caleb, "VEGFR-2 and VEGFR-3 Expression as a Function of Jagged-1 Over-Expression in HUVEC Cells" (2014). Pepperdine University, Featured Research. Paper 142.
https://digitalcommons.pepperdine.edu/sturesearch/142