摘要
Exposure to crystalline silica is considered to increase the risk for lung fibrosis.Although the molecular mechanisms of pathogenesis and progression of silicosis is not clear,the myofibroblast which is the primary effector cell plays an important role.We aim to study the genome-wide DNA methylation profiles of lung fibroblast which is co-culture with alveolar exposure to crystalline silica in vitro.In this study,SiO_2 exposure fibroblast methylome analysis identifies extensive epigenetic changes involved in several signaling pathways,such as MAPK signaling pathway and metabolic pathways.We also found several candidates such as Tgfb1,Fgf6,Mapk9 and Tab1 in order to explore the mechanism of myofibroblast differentiation.The genome-wide DNA methylation profiles of fibroblast in experimental silicosis model will be useful for future studies on epigenetic gene regulation in fibroblast differentiation.
Exposure to crystalline silica is considered to increase the risk for lung fibrosis.Although the molecular mechanisms of pathogenesis and progression of silicosis is not clear,the myofibroblast which is the primary effector cell plays an important role.We aim to study the genome-wide DNA methylation profiles of lung fibroblast which is co-culture with alveolar exposure to crystalline silica in vitro.In this study,SiO_2 exposure fibroblast methylome analysis identifies extensive epigenetic changes involved in several signaling pathways,such as MAPK signaling pathway and metabolic pathways.We also found several candidates such as Tgfb1,Fgf6,Mapk9 and Tab1 in order to explore the mechanism of myofibroblast differentiation.The genome-wide DNA methylation profiles of fibroblast in experimental silicosis model will be useful for future studies on epigenetic gene regulation in fibroblast differentiation.
引文