Injury, Repair, and Regeneration
Advancing knowledge about developmentally sensitive stages of cellular, tissue, and organ responses to injury and investigating the capacity of early life cells, tissues, and organs for repair and regenerative processes that may be applied to diseases throughout the lifespan.
The Gosain Plastic Surgery and Craniofacial Biology Laboratory is using a porcine model to study how tissue deformation impacts cell responsiveness and adaptation to stress, how these microscopic events relate to growth at the tissue level, and to predict this adaptation through computational modeling. This study will allow us to expand our understanding of tissue expansion, a common technique for breast reconstruction in post-mastectomy breast cancer patients. Additionally, the lab is using a zebrafish model and primary cell culture to study the mechanisms behind craniosynostosis, a condition in which the bones of the cranial vault fuse prematurely. The goal of this study is to increase our understanding of the genetic determinants of craniosynostosis.
We study the roles that mitochondria play in development, health, and disease. In addition to their established role in bioenergetics, mitochondria regulate many cell processes by contributing to the biosynthesis of nucleic acids, lipids, and proteins. They also control cell responses to stress by signaling via the release of reactive oxygen molecules to the cytosol. Mitochondria also participate in signaling through their uptake or release of ionized calcium. Mitochondria are involved in multiple functions related to signaling through their generation of metabolic substrates involved in protein (including histone) methylation and demethylation, as well as protein acetylation and deacetylation. We study these functions with particular interest in perinatal disorders associated with prematurity, as well as in cardiopulmonary diseases. Finally, we investigate how mitochondrial functions affect tumorigenesis and tumor phenotypes in cancer.
The Zhao Laboratory studies the molecular mechanisms of endothelial injury and regeneration, resolution of inflammation, and obliterative vascular remodeling in the pathogeneses of sepsis, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and pulmonary arterial hypertension (PAH).
Recovery of endothelial barrier integrity after vascular injury is vital for endothelial homeostasis and resolution of inflammation. Endothelial dysfunction plays a critical role in the initiation and progression of vascular diseases such as ALI/ARDS and atherosclerosis. A part of the research in the lab, employing genetically modified mouse models of human diseases, endothelial progenitor cells/stem cells, and translational research approach as well as nanotechnology, is to elucidate the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury and determine how aging and epigenetics regulate these processes (J. Clin. Invest. 2006, 116: 2333; J. Exp. Med. 2010, 207:1675; Circulation 2016, 133: 2447). We are also studying the role of endothelial cells in regulating macrophage functional polarization and resolving inflammatory lung injury. These studies will identify druggable targets leading to novel therapeutic strategies to activate the intrinsic endothelial regeneration program to restore endothelial barrier integrity and reverse edema formation for the prevention and treatment of ARDS in patients.