RNA Details
                    Disease Name
                    
                    idiopathic pulmonary fibrosis
                    
                    Tissue
                    
                    lung
                    
                    RNA Symbol
                    
                    miR-497a-5p
                    
                RNA ID
                    
                    
                    
                RNA Type
                    
                    miRNA
                    
                Alteration Pattern
                    
                    up regulation
                    
                Species
                    
                    mus musculus
                    
                Detection Methods
                    
                    qRT-PCR; Dual-luciferase reporter assay;  etc.
                    
                Target
                    
                    Reck
                    
                Pathway
                    
                    NA
                    
                PubMed ID
                    
                    
                    
                    
                    
                Title
                    
                    The role of miR-497-5p in myofibroblast differentiation of LR-MSCs and pulmonary fibrogenesis
                    
                Year
                    
                     2017
                    
                Function
                    
                    "MiR-497-5p was significantly upregulated both during myofibroblast differentiation of lung resident mesenchymal stem cells (LR-MSCs) and in the lung tissues of a pulmonary fibrosis model. Reversion-inducing cysteine-rich protein with kazal motifs (Reck) was one of the target genes of miR-497-5p, and Reck could suppress the expression of matrix metalloproteinase-2 (Mmp2) and Mmp9, which could activate latent transforming growth factor-B1 (TGF-B1). Upregulation of miR-497-5p could induce LR-MSCs to differentiate into myofibroblasts and promote pulmonary fibrogenesis, while inhibition of its expression could effectively retard these processes."