Mentor: Dr. Jae-Sung Kim
College of Medicine, Department of Surgery
"I applied to the University Scholars Program in order to gain experience presenting my research in a more formal setting. I hope to improve my skills giving short snapshot presentations about my research project. This year, I also hope to collect enough data to be able to draw conclusions in a senior thesis, and graduate with honors in my college."
Microbiology and Cell Science
National Merit Finalist, 2009
Robert C. Byrd Honors Scholar, 2009
Anderson Scholar of High Distinction, 2011
Hobbies and Interests
love Learning New Songs
Piano (15 years)
Novel Modulation of the Autophagic Pathway by Desipramine
Liver disease represents a major health problem in the United States, where there are over 5.5 million cases. Advances in liver transplantation have led to better survival rates for recipients, but the benefits of this procedure are limited by a shortage of donor livers. In fact, only about 27% of those on the waiting list are able to receive a donor liver. Livers that are not used in transplantation are often deemed marginal due to preexisting pathological conditions such as hypotension, hepatitis C, ischemia, aging, or other metabolic dysfunctions. Salvation of these marginal livers would significantly increase the donor pool for patients with end-stage liver diseases. One potential mechanism to salvage marginal livers is autophagy, a cellular process that selectively eliminates damaged proteins and dysfunctional organelles. Although Rapamycin and its derivatives can induce autophagy by inhibiting the mTOR complex, clinical application of Rapamycin is limited due to its immunosuppressive activity. The identification of additional drugs that enhance autophagy without compromising the immune system is needed. Preliminary studies have shown that Desipramine, an FDA approved tricyclic antidepressant, to be an effective enhancer of autophagy in primary mouse hepatocytes. This study will characterize the mechanism of Desipramine in autophagy stimulation. Specifically, various stages of autophagy will be analyzed to determine which stage(s) of autophagic machinery is affected by Desipramine. First, we will determine whether Desipramine can stimulate hepatic autophagy. Second, we will investigate the cellular mechanisms of autophagy induction by Desipramine, and will determine whether Desipramine induces autophagy through an mTOR-dependent or independent signaling pathway. Ischemia/reperfusion (I/R) injury is a key mechanism underlying pathological outcomes after liver transplantation. Marginal livers are substantially sensitive to I/R injury, compared to normal livers. Accordingly, we will test whether Desipramine protects the liver against (I/R) injury.