Carl Hansen joins the Biology Department from Bloomsburg University of Pennsylvania. He earned a M.A. in Zoology from the University of Maine in Orono, received a Ph.D. in Physiology from Penn State’s Hershey Medical Center and obtained postdoctoral training in the Department of Biochemistry and Biophysics at the University of Pennsylvania. Subsequently, he spent 10 years as an AHA- and NIH-funded researcher at the Weis Center for Research at Geisinger Clinic before moving to his 18 yr. career at the Bloomsburg University.
Dr. Hansen's research experiences involve studying energy metabolism in hagfish hearts, characterizing cardiac muscle compensatory mechanism activated post-myocardial infarction, elucidating the inositol phosphate metabolic pathway and its integration with Ca2+ signaling, and understanding the roles of heterotrimeric G-proteins in specifying G-protein coupled receptor signaling functions using zebrafish and mouse models. Hansen has also been engaged in program building. He spear-headed the development of a molecular biology option at BU by obtaining an NSF-CCLI grant along with new course development in bioinformatics and genomics. He co-developed an undergraduate certificate program in genetic counseling and genomic research that prepares students to enter master programs in genetic counseling.
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.
