Konstantinos Kontodimas

I moved from Greece in 2016 to do my B.S in molecular biology at Boston university. During my time at BU, I worked under Dr. Bosmann at the Pulmonary department studying macrophage biology and their role in respiratory infections. I continued working at the Bosmann lab as a research assistant, studying innate antiviral immunity using transgenic mouse models and sepsis. As a graduate student in the Varelas lab, I study the epithelial, endothelial and mesenchymal changes that happen in the lung after injury.

The perturbation of homeostasis in the lung has been associated with some of the most prevalent pulmonary disorders such as fibrosis and emphysema. The recent emergence of SARS-CoV-2 has highlighted the need to better understand how epithelial and endothelial dysregulation can contribute to the severity and outcome of certain diseases and infections. The mesenchyme, which is speculated to bridge the lung epithelium with the vasculature, has been extensively studied in the context of disease due to its bivalent role during injury response, . In order to properly dissect the contribution of fibroblasts in disease onset, we need to first decipher what leads these cells to deviate from homeostasis. YAP and TAZ are two transcriptional mediators that fall under the Hippo protein family and have been shown to play a role in homeostatic regulation in many different organ systems, especially the mesenchyme. There are several studies that highlight the importance of YAP and TAZ in proper epithelial, endothelial, and mesenchymal co-functioning, however the mechanism by which the dysregulation of these proteins contributes to pathology still remains a mystery.