Thursday, January 25, 2018

URSP Student Luc Tran Researches Idiopathic Pulmonary Fibrosis

My project for this fall semester is a continuation of my last semester OSCAR project. The overall theme of my research is a disease known as idiopathic pulmonary fibrosis (IPF). IPF is a fatal lung disease that is characterized with scarring of the lung overtime due to over activation of fibroblasts and increased collagen deposition. My interest in IPF began when I was able to join Dr. Geraldine Grant’s lab during the Biology Research Semester. My project last semester was to determine the effect of exposure of a metabolite of acetaminophen, known as N- acetyl benzoquinone imine (NAPQI) on the expression of certain IPF gene markers: alpha smooth muscle actin (ASMA) and collagen-1-alpha (COL1A). I found that direct NAPQI exposure had no significant increase in ASMA or COL1A in both normal and IPF fibroblasts. However, there was an increase in the expression of Procollagen-Lysine,2-Oxoglutarate 5-Dioxygenase 1 and 2 (PLOD1/2) in the IPF fibroblasts. My experiment this semester is to expose epithelial cells to acetaminophen so that the epithelial cells can metabolize acetaminophen into NAPQI and transfer the NAPQI to the fibroblasts. My goal is to verify my data from the summer, regarding changes in expression of PLOD1/2. This finding would begin to provide an explanation linking IPF with acetaminophen consumption because direct cause of IPF is still unknown.

On a daily basis, I culture the fibroblasts and also run q-PCRs to determine expression of ASMA, PLOD1 and PLOD2. I discovered a significant increase in PLOD1 in the IPF fibroblasts as I did with direct exposure to NAPQI. This project is related to my long term goal of going to medical school by that it is direct research on a disease and also if I can link acetaminophen to IPF, I can warn my future patients about the dangers of acetaminophen.