Graduate student awarded T32 grant for lung cell injury and repair research

Jon Fritz, a white male, stands in the lab working on his research
Jon Fritz in the lab

Graduate student, Jon Fritz is one of the six recipients of the T32 Predoctoral Research Training Grant from The Ohio State University Center for Clinical and Translational Science (CCTS) for his research on lung cell injury and repair.

The T32 is a new award funded by a five-year $1.5M NIH grant to fund graduate student training in clinical and translational research. This predoctoral training program leverages the large, collaborative and multidisciplinary research environment at Ohio State University to increase the reach of clinical and translational science education and training across campus and to recruit and develop a diverse cohort of learners to become the next generation of clinical and translational scientist-leaders.

Fritz’s co-advisor in Biomedical Engineering, Samir Ghadiali, PhD shared his enthusiasm over Fritz’s T32: “It is very exciting that Jon won this award. Because CCTS is focused on clinical translation, it typically funds those who are either earning MDs or enrolled in a health science college. As a Biophysics graduate student who is co-advised by College of Engineering (Ghadiali) and College of Medicine (Englert) faculty members, Jon is unique among his T32 cohort and his winning this award speaks to the real potential of his work which combines engineering tools in my lab with clinical applications in Dr. Englert’s lab to develop new therapies for pulmonary disorders.”

Jon Fritz is the only recipient of the award’s first cohort from the College of Engineering. He was funded through the T32 for his project titled “Preventing Lung Cell Membrane Injury During Mechanical Ventilation by Targeting mTORC1-Dependent Phosphorylation of Annexin A2”, described in detail below.

Fritz’ project explores ways to mitigate lung injury from mechanical ventilation for those with acute respiratory distress syndrome (ARDS). ARDS is the leading cause of lung injury in ICU patients. While the standard of care for treating ARDS is mechanical ventilation, this artificial ventilation can damage the membranes or barriers of lung cells.

Our understanding of how lung cells repair their membranes during mechanical ventilation is limited, which is a key reason why there are no therapeutics for ARDS. Our data demonstrate that a protein involved in the repair of cell membranes (Annexin A2) may play an important role in protecting lung cells during mechanical ventilation. By using a combination of biophysical methods and biomedical engineering devices, we hope to understand how lung cells repair after injury and thereby expand the pool of therapeutic targets for mitigating lung injury to ARDS patients.

Congratulations to Jon Fritz for this exciting accomplishment. We look forward to seeing how your research improves human health!