Dr. Hansen’s current research focuses on understanding G-protein mediated signaling inputs regulating angiogenesis. Angiogenesis is the process whereby new blood vessels sprout from preexisting vessels. This process requires endothelial cells to make cell fate decisions regulating growth, maturation, and quiescence of the newly formed vessels. Although important for physiologic situations such as wound healing, dysregulation of angiogenic signaling cascades contribute to many pathologic conditions including retinopathy, atherosclerosis, pulmonary dysfunction, and cancer. A growing body of evidence supports the involvement of G-proteins as both positive and negative regulators of the angiogenic process. Interestingly, Gng11-/- mice exhibit vessel overgrowth in the mouse retinopathy model. Endothelial cells lacking the Gγ11 protein exhibit delayed cell cycle exit and resumption of the quiescent state. These cell cycle changes are associated with altered Yap/Taz and Foxo1/3 transcriptional networks that control the switch between proliferation and quiescence. Based on these and other data, it is hypothesize that the Gγ11 protein functions as an angiostatic switch to promote and maintain endothelial quiescence. Although largely dispensable under homeostatic conditions, we speculate that the Gγ11 protein is critical for applying the “brake” that prevents pathologic angiogenesis. This research project is a collaborative effort with the laboratory of Dr. Janet Robishaw.
