Impacts of TRIM72 on bleomycin-induced injury and pulmonary fibrosis; an in-vitro approach.
Date
April 2022
Location
Schewel 208
Description
Idiopathic Pulmonary Fibrosis is a chronic, progressive disease of the lungs where thick scar tissue develops irreversibly, leading to dyspnea and respiratory failure. Previous studies have implicated lack of functioning alveolar type 2 epithelial (AT2) cells in IPF pathogenesis, with some pointing to tripartite motif protein 72 (TRIM72) as a critical component for acute plasma membrane damage repair for AT2 cells. This study tested the effects of TRIM72 on in-vitro cultured rat lung epithelial (RLE) cells with idiopathic pulmonary fibrosis. In this study, we tested and compared the effect of bleomycin in RLE cells with or without TRIM72 expression. We examined the expression of Nox4 (a marker for oxidative stress) and P21 (a marker for cell senescence) using immunoblot. We found an increase in both Nox4 and P21 in response to bleomycin treatment. RLE cells overexpressing TRIM72 had reduced levels of Nox4 and P21 as compared to RLE cells lacking TRIM72 after bleomycin exposure. Further research is being conducted on examining the levels of other senescence markers, as well as in the effects of externally introduced TRIM72 (recombinant) on bleomycin induced injury in RLE cells.
Presentation Type
Presentation
Impacts of TRIM72 on bleomycin-induced injury and pulmonary fibrosis; an in-vitro approach.
Schewel 208
Idiopathic Pulmonary Fibrosis is a chronic, progressive disease of the lungs where thick scar tissue develops irreversibly, leading to dyspnea and respiratory failure. Previous studies have implicated lack of functioning alveolar type 2 epithelial (AT2) cells in IPF pathogenesis, with some pointing to tripartite motif protein 72 (TRIM72) as a critical component for acute plasma membrane damage repair for AT2 cells. This study tested the effects of TRIM72 on in-vitro cultured rat lung epithelial (RLE) cells with idiopathic pulmonary fibrosis. In this study, we tested and compared the effect of bleomycin in RLE cells with or without TRIM72 expression. We examined the expression of Nox4 (a marker for oxidative stress) and P21 (a marker for cell senescence) using immunoblot. We found an increase in both Nox4 and P21 in response to bleomycin treatment. RLE cells overexpressing TRIM72 had reduced levels of Nox4 and P21 as compared to RLE cells lacking TRIM72 after bleomycin exposure. Further research is being conducted on examining the levels of other senescence markers, as well as in the effects of externally introduced TRIM72 (recombinant) on bleomycin induced injury in RLE cells.