URSP Student Isabella Meerzaman Investigates whether BAX or Bax Inhibitor 1 (BI-1) suppresses Endoplasmic Reticulum (ER) stress induced cell death in Idiopathic Pulmonary Fibrosis

Clinical research has led to novel treatment options that offer patients a glimmer of hope by improving and extending their quality of life. The ability of scientists and researchers to map disease-causing pathways to identify inhibitors/activators that slow or stop disease progression has provided the medical community with a new treatment arsenal. Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease that affects 3 million individuals globally. IPF causes excessive permanent scarring of the lungs known as fibrosis, making it hard for proper gas exchange to occur.

I have been working in Dr. Grants lab focusing on a project that investigates whether “BAX or Bax Inhibitor 1 (BI-1) suppresses Endoplasmic Reticulum (ER) stress induced cell death in Idiopathic Pulmonary Fibrosis.”. ER stress is induced in IPF cells, then BI-1, BAX or both are silenced to see if sensitivity to ER stress is altered. If BI-1 or BAX can suppress ER stress induced cell death, it could critically alter IPF treatment and provide a possible pathway framework to target. This project has allowed me to gain more experience with bench based lab research and data analysis. Working in Dr. Grants lab has helped prepare me for my post bacc research fellowship with the Department of Defense and my future career as a clinical research physician.