Infections

Abstract

bAsic reseArch on biocomPAtibility, immunology, inflAmmAtion And fibrosis miRNA589 Regulate Epithelial-Mesenchymal Transition in Human Peritoneal Mesothelial Cells Background: microRNAs (miRNA, miR) are thought to interact with multiple mRNAs resulting in either translational repression or degradation which is involved in the EMT process. Since miRNAs distributed with tissue specificity, the role of miRNAs in peritoneal fibrosis remains unknown. Our unpressed data showed that expression of miRNA589 was notably decreased in HPMCs isolated from patients undergoing long-term continuous ambulatory peritoneal dialysis (CAPD). Objective: To determine if miRNA589 regulates the EMT induced by TGFβ1 in human peritoneal mesothelial cell line (HMrSV5 cells). Methods: HMrSV5 cells were divided into three groups: control group (only FBS-free DMEM/F12), TGF-β1 group (treated with TGF-1 5 ng/ml for 24h) and pre-miR-5891 group (pre-treated with pre-miR-589 to up-regulate the level of miR-589, and treated with TGF-1 5 ng/ml for 24h). The level of miRNA589 was determined by realtime PCR. The expressions of ZO-1, vimentin, E-cadherinin HPMCs were determined by immunofluorescence, realtime PCR, and Western blot, respectively. Result: In vitro,TGF1 led to up-regulation of vimentin and downregulation of ZO-1 as well as E-cadherin in HMrSV5 cells, which suggested EMT was induced. The changes were accompanied with notably decreased level of miRNA589 in HMrSV5 cells treated by TGF1. Over-expression of miRNA589 by transfection with pre-miRNA589 partially reversed these EMT changes. Conclusion: miRNA589 mediates TGF1-induced EMT in human peritoneal mesothelial cells.