Interaction between pancreatic islets and vascular endothelial cells is necessary for the maintenance of beta-cell mass and function. Aside from acting as a conduit for molecular oxygen, vascular endothelial cells in vivo secrete the majority of islet extracellular matrix (ECM). This ECM likely provides a permissive signal for beta-cell proliferation, contributing to the coordinated hyperplasia of these tissues during the early stages of Type 2 diabetes. This ECM also provides a reservoir for heparin binding growth factors that further modulate this hyperplasia, including fibroblast growth factor (FGF) and vascular endothelial growth factor-A (VEGF-A). We hypothesize that communication between beta-cells and vascular endothelial cells directs the proliferation and function of both tissues.
To examine beta-cell-vascular endothelial cell interaction, my lab uses a number of cutting-edge techniques: two-photon excitation microscopy, confocal microcopy, microfluidics, and live cell imaging of fluorescent proteins. Current projects use cell culture and ex vivo pancreatic islet models. These studies will advance our understanding of pancreatic islet communication, with a specific focus on the communication between beta-cell and vascular endothelial cells through FGF/FGFR1-signaling.