My project for this summer 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 find a similar increase in PLOD1 and PLOD2 after “co-culture” treatment of the
normal and IPF fibroblasts with acetaminophen as direct exposure to NAPQI. 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.
