Antifibrotic Effect Of Mir-29b In The Process Of Epithelial-mesenchymal Transition In Idiopathic Pulmonaryfibrosis

Background and ObjectiveIdiopathic pulmonary fibrosis(IPF) is a diffuse interstitial lung disease in a special type, is an unexplained, in adults, confined to the lung, progressive fibrosing interstitial pneumonia.This disease can be characterized by alveolar epithelial cell injury, the failure of re-epithelialization leading to epithelial-mesenchymal transition(EMT), inflammatory cell infiltration, fibroblast hyperplasia, deposition of extracellular matrix(ECM), and scar formation.micro RNA(mi RNA) is a type of length 19 to non-coding RNA 25 nt small molecules by specifically binding to the target gene sequence 3’-UTR region of the gene expression and regulation, and thus participate in a variety of physiological and pathological processes, including cell proliferation, differentiation and apoptosis and carcinogenic and other processes.In recent years, mi RNA and gene expression and regulation of organ fibrosis become a hot topic for clinical targeted therapy offers the possibility of organ fibrosis.mi R-29 b is a tightly associated with fibrotic diseases mi RNA, plays an important role in the regulation of multiple organ fibrosis, including the heart, liver, lung fibrosis.In this study, the mi R-29 b mimic transfected into alveolar epithelial cells, research antifibrotic effect of mi R-29 b by up-regulate expression in the process of epithelial-mesenchymal transition in idiopathic pulmonary fibrosis.Methods 1. IMR-90 cells cultured in vitro were induced by 2 μg/L TGF-β1. 2. To assay the expression of the markers of epithelial cell and mesenchymal cell byReal-time PCR and Western blot, and to observe the cellular morphologicalchanges before and after IMR-90 cells being induced by TGF-β1 by invertedphase contrast microscope. 3. Transfection with mi R-29 b mimic. 4. To assay the expression of the markers of epithelial cell and mesenchymal cell byReal-time PCR and Western blot, and to observe the cellular morphologicalchanges. 5. SPSS 17.0 was used to analyze all the dates. The ANVOA was used to analyzethe comparison among more groups. The LSD-t was used to analyze thecomparison two groups. Results 1. TGF-β1-induced cells from normal or polygonal shaped pebble into a spindle,spindle, intercellular connections become loose, showing mesenchymal cellmorphology; mi R-29 b transfected cell morphology contrast TGF-β1-inducedcells there are significant changes in morphology, showing similar pebble-shapedor polygonal epithelial morphology, and cell morphology NC group continued toshow a mesenchymal cell morphology, compared to TGF-β1-induced group hadno significant change. 2. By Western blot and Real-time PCR analysis,E-cadherin expression significantlydecreased and α-SMA, p-Smad3 and COL1A1 expression significantly increasedin IMR-90 cells induced with TGF-β1 compared with negative controls(P<0.01). 3. After transfection with mi R-29 b mimic, E-cadherin expression was increased andα-SMA, p-Smad3 and COL1A1 expression were decreased than before(P<0.01). ConclusionUpregulation of mi R-29 b may inhibit the TGF-β1/Smad3 signaling pathway mediate epithelial-mesenchymal transition, and delay the progression of idiopathic pulmonary fibrosis.