• 200 Lothrop Street, W1206A BST Pittsburgh, PA 15261
  • (412) 383-5774
  • wangx17@upmc.edu

XINGAN WANG, MD, PhD

Assistant Professor of Medicine

Education:
MD, Tongji University School of Medicine, Shanghai, China; PhD, The Second Military Medical University, Shanghai, China

My research interest is “bridging” the bench and the bedside in two areas of lung transplantation: ischemia-reperfusion (I/R) injury and transplant rejection/tolerance. Before being a full-time researcher in 2011, I had worked as a surgeon in Shanghai Pulmonary Hospital, the largest lung surgery center in China, for 11 years. Therefore, I know what both sides need.

On the one hand, I take surgical skills and clinical knowledges from bedside to bench. A stereotype is that 18 hours of cold ischemia at 0°C is sufficient to trigger severe I/R injury in mouse model of lung transplantation. As a matter of fact, both structure and function of the grafted lung are almost normal even if the cold ischemia time is prolonged to 24 hours. The virtual I/R injury would be obscured if too much collateral damage has occurred during surgical procedures. Multiphoton fluorescence microscopy allows to image living mouse tissue/organ at the cellular level, but it’s hard to stabilize a mouse lung without impairing its circulation and ventilation. I solved this problem and went further to initiate a new serial imaging technique, “Chest Window”, in which a portion of left chest wall is replaced by a piece of glass with thickness of 0.19 mm. I also pioneered a combined model of Ex vivo lung perfusion (EVLP) and lung transplantation in mice.

On the other hand, I channel the new basic scientific knowledge into preclinical applications. Neutrophil extracellular traps (NETs) are newly found to be involved in many acute or chronic injuries. In a study supported by 2015 Norman E. Shumway Career Development Award, we visualized NETs and revealed a critical mechanism of I/R injury and rejection in mouse lung transplants. The ongoing study is expected to yield insights into the mechanism of necroptosis, a programmed form of necrosis, in lung I/R injury.

Publications