"I applied to the university scholars program for the opportunity to work in a lab environment. I hope to learn laboratory techniques that are otherwise unavailable to an undergraduate student. My goal for this year is use the techniques and apply them to my current hypothesis as I study the mechanistic pathways of Intimal Hyperplasia Development."
Microbiology and Cell Science
My primary interest are in cell biology; learning the physiology and genetics of microorganisms. My current research is on vascular tissue with the primary focus on Intimal Hyperplasia.
Academic and Other Awards
- University Scholars Program Scholarship (2011-2012)
- International Baccalaureate
- Florida Bright Futures (2009)
- College of Liberal Arts and Sciences Dean's List (2010)
- President's Honor Roll (2011)
- Dancing Gators
- Health Educated Asian Leaders
- Intramural Soccer and Volleyball
I have volunteered at Shands Hospital through the NICU.
Hobbies and Interests
- Outdoors, soccer, running, volleyball, knitting, and playing guitar.
KLF2 Interaction with TGF- β And 1 IL-1 Signaling Pathways In Smooth Muscles Cells
Heart attacks and strokes due to arterial blockages remain an unresolved issue causing death and disability in the United States. Clinically, arterial blockages can be treated with surgical procedures such as bypass vein grafts. They are often not long-term solutions because of intimal hyperplasia (IH), a thickening of the intima layer of blood vessels, generally caused by damage of endothelial cell layer. This thickening of the intima often leads to a re-closing or occlusion of the vessel. Dr. Berceli’s lab is devoted to understanding the mechanism and identifying key regulatory proteins that promote IH. The Berceli lab has already identified the cytokines transforming growth factor β (TGF-β) and interleukin 1 (IL-1), both of which aid in inflammation. The lab has also observed increased levels of the transcription factor Kruppel Like Factor 2 (KLF2); however its role in IH development has not yet been established. KLF2 has been shown to be an important down-regulator of both the IL1 and TGF-β signaling pathways in human umbilical vein endothelial cells (HUVECs). Using an adenovirus that is designed to overexpress KLF2, I will study the interaction of KLF2 with IL1 and TGF- β signaling pathways in smooth muscle cells. Cultured smooth muscle cells will be transfected with either KLF2 adenovirus or control virus. 24 hours following transfection, the cells will be stimulated with IL1, TGF-β, or control media. We will assess proliferation of these cells using a Ki-67 proliferation kit and a Qiagen kit followed by real time PCR to look at changes in gene expression. If KLF2 interacts with IL1 and TGF-B, there will be decreased proliferation. We also anticipate KLF2 will down regulate genes that are normally upregulated in response to KLF2. Negative results would indicate that KLF2 does not interact with these cytokines in proliferation or other inflammatory pathways.