Ashleigh Kilgore
Pronouns: she/her/hers
Research Mentor(s): Thomas Sisson
Research Mentor School/College/Department: Internal Medicine / Medicine
Program: UROP
Session: Session 7 (4:40pm – 5:30pm)
Authors: Thomas Sisson, Ashleigh Kilgore
Abstract
Despite the vast amount of scientific knowledge about pulmonary fibrosis, a chronic illness characterized by scarring of the lung, the detailed mechanisms that cause this disease require further study. One protein of particular interest in promoting lung fibrosis is Plasminogen Activator Inhibitor (PAI-1). This protein causes lung scarring in multiple animal models but the specific cellular effects that cause the scarring are unknown. In this study, we hypothesized that PAI-1 would activate fibroblasts, the key cell that produces scar. To test this hypothesis, human fibroblast cells were grown in a low glucose medium until the proper confluency was reached. Then, the cells were serum starved and further treated with the pro-fibrotic growth factor TGF-ß. These cells were then lysed and analyzed to assess their profibrotic response. Following a repetition of this process, PAI-1 will be inhibited and the effects of that inhibition will be examined on the TGF-ß induced pro-fibrotic response . The analysis of PAI-1, including its effects on the cells while it’s both active and inhibited, will allow us to fully understand the mechanism that creates the scarring within the lung of a person that has pulmonary fibrosis. By proving that PAI-1 is required for cells to be pro-fibrotic in nature, we can further investigate its specific function within cells. Ultimately, understanding and establishing the mechanism by which the lung scars can aid in scientific movements towards more efficient treatments for those with pulmonary fibrosis.
