BYU

Abstract by Rebecca Viazzo

Personal Infomation


Presenter's Name

Rebecca Viazzo

Degree Level

Doctorate

Abstract Infomation


Department

Chemistry and Biochemistry

Faculty Advisor

Pam Van Ry

Title

avB6 Inhibitor Improves Idiopathic Pulmonary Fibrosis Outcomes

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is an interstitial lung disease that causes lung fibrosis leading to ineffective oxygen exchange to the blood. Once diagnosed, IPF is fatal within 3-5 years. There is no known cause or treatment that improves outcomes. Although the cause is unknown, it is speculated that the TGFB cell signaling pathway is responsible for the chronic inflammation and fibrosis characteristic of IPF. avb6 integrin is an upstream activator of the TGFB  pathway and a therapeutic target. We prove that our avB6 inhibitor, AG2, halts fibrosis in the standard IPF mouse model that uses bleomycin to induce fibrosis in lungs. Fibrosis progression is evaluated through quantifying weekly uCT scans and Masson-Trichrome stained lung sections. Lung sections and uCT scans show lung fibrosis is significantly lower in bleomycin-plus-AG2-treated mice as compared to mice treated with bleomycin alone. This suggests AG2 is a promising therapeutic to improve outcomes of IPF patients.