Project description:We found strong protein-protein interactions within these dysregulated genes in nintedanib treated IPF fibroblast, with most genes involved in the pathways of cell cycle, mitotic cell cycle, and cell division. In IPF fibroblasts, we found nintedanib treatment was associated with downregulation of has-miR-92a-1-5p, which might de-repress SLC25A23 expression, and upregulation of has-miR-486-5p, which might repress DDX11, E2F1, and PLXNA4 expressions.
Project description:We found strong protein-protein interactions within these dysregulated genes in nintedanib treated IPF fibroblast, with most genes involved in the pathways of cell cycle, mitotic cell cycle, and cell division. In IPF fibroblasts, we found nintedanib treatment was associated with downregulation of has-miR-92a-1-5p, which might de-repress SLC25A23 expression, and upregulation of has-miR-486-5p, which might repress DDX11, E2F1, and PLXNA4 expressions.
Project description:To investigate the mechanisms underlying disease progression in idiopathic pulmonary fibrosis (IPF), we obtained lung fibroblasts from IPF patients from both non-fibrotic and fibrotic areas, and compared gene expression between these areas by DNA microarray. Forty-two genes were commonly upregulated more than two-fold in fibroblasts from the fibrotic lung region compared with their counterparts from the non-fibrotic region in all three IPF patients.
Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and highly lethal lung disease with unknown etiology and poor prognosis.