ABSTRACT
Objective To investigate the important role of angiogenin-like protein 4 (Angptl4) in pulmonary fibrosis and to provide a new therapeutic targets for pulmonary fibrosis.Methods We established the pulmonary fibrosis animal models in rat by tracheal instillation of bleomycin.Then,we detected the expression of Angptl4 through real-time polymerase chain reaction (RT-PCR) and Western Blot.Rat lung fibroblast (RLF) was transfected into Angptl4-shRNA plasmid.Then we detected the changed collagen expression in RLF cells after transfection through RT-PCR and Western blot.Results The expression of Angptl4 was up-regulated in the bleomycin-induced rat pulmonary fibrosis model.The expression of both collagen Ⅰ and collagen Ⅳ in RLF cells transfected with Angptl4-shRNA plasmids were down-regulated compared with control after TGF-β treatment.Conclusions Inhibiting the expression of Angptl4 can reduce the expression of collagen fibers in lung tissue,then delaying the progression of pulmonary fibrosis.
ABSTRACT
Objective To investigate the expressions of microRNA-221 (miR-221) in the human pulmonary fibrosis tissues and in adenocarcinoma(A549) cells treated with transforming growth factor beta 1 (TGFβ1).Methods Real time-PCR was used to detect the expressions of miR-221 in pathologically diag nosed as pulmonary fibrosis tissue and in A549 cells treated with TGFβ1.Results miR-221 in pulmonary fibrosis tissue was downregulated compared to normal tissues (P ＜ 0.05).The morphology of cells was changed from long spindle type to short, the number of cells was increased, and the adjacent cells were not connected closely.TGFβ1, N-cadherin, vimentin, α-smooth muscle actin (α-SMA), collagen Ⅰ, and collagen Ⅲ levels were higher, whereas E-cadherin level was lower in TGFβ1-treated group compared to the control group.miR-221 expression was downregulated in cells after TGFβ1 treatment (P ＜ 0.05).Conclusions miR-221 was downregulated in pulmonary fibrosis tissues and in A549 cells, which indicates that miR-221 may play an important role in the formation of pulmonary fibrosis.