Fang, Jennifer
Assistant Professor
y long-term research interest is to study healthy blood vessel development and remodeling, and to use both microphysiological organ-on-a-chip systems as well as transgenic mouse models to understand how intercellular signals – including, those involving gap junctions and their constituent proteins (connexins, Cx) – regulate these processes. I am also interested in developing transgenic mouse models as well as microphysiological disease models of vascular malformation to elucidate how dysregulation of cell-cell signaling contributes to blood vessel disorganization, such as in the rare congenital disorder Hereditary Hemorrhagic Telangiectasia (HHT) for which no cure is currently available. In prior work, I found that connexins regulate endothelial proliferation and large vessel remodeling, as well as vasodilatory and inflammatory responses, in a model of peripheral ischemia. Later, I identified the novel flow-activated Notch Cx37-p27 signaling axis that arrests endothelial cell cycle to enable arterial specification during blood vessel development. In my current work, I have developed the first organ-on-a-chip model for HHT. In future work, I will use this HHT-on-a-chip model and other microvasculature-on-a chip models as well as mouse models to study the underlying physiology of angiogenesis, vessel remodeling, and HHT-related vascular malformations, with the goal of helping to identify a cure for HHT and other diseases involving pathological vessel growth.
Biography
y long-term research interest is to study healthy blood vessel development and remodeling, and to use both microphysiological organ-on-a-chip systems as well as transgenic mouse models to understand how intercellular signals – including, those involving gap junctions and their constituent proteins (connexins, Cx) – regulate these processes. I am also interested in developing transgenic mouse models as well as microphysiological disease models of vascular malformation to elucidate how dysregulation of cell-cell signaling contributes to blood vessel disorganization, such as in the rare congenital disorder Hereditary Hemorrhagic Telangiectasia (HHT) for which no cure is currently available. In prior work, I found that connexins regulate endothelial proliferation and large vessel remodeling, as well as vasodilatory and inflammatory responses, in a model of peripheral ischemia. Later, I identified the novel flow-activated Notch Cx37-p27 signaling axis that arrests endothelial cell cycle to enable arterial specification during blood vessel development. In my current work, I have developed the first organ-on-a-chip model for HHT. In future work, I will use this HHT-on-a-chip model and other microvasculature-on-a chip models as well as mouse models to study the underlying physiology of angiogenesis, vessel remodeling, and HHT-related vascular malformations, with the goal of helping to identify a cure for HHT and other diseases involving pathological vessel growth.
