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Updated: May 17, 2026
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
miRNA589 regulates epithelial-mesenchymal transition in human peritoneal mesothelial cells
Ke Zhang1, Hao Zhang, Xun Zhou
1Department of Nephrology and Renal Institute, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, China.
Abstract:
Background. microRNA (miRNA, miR) are thought to interact with multiple mRNAs which are involved in the EMT process. But the role of miRNAs in peritoneal fibrosis has remained unknown. Objective. To determine if miRNA589 regulates the EMT induced by TGFβ1 in human peritoneal mesothelial cell line (HMrSV5 cells). Methods. 1. Level of miR589 was detected in both human peritoneal mesothelial cells (HPMCs) isolated from continuous ambulatory peritoneal dialysis (CAPD) patients' effluent and HMrSV5 cells treated with or without TGFβ1. 2. HMrSV5 cells were divided into three groups: control group, TGFβ1 group, and pre-miR-589+TGFβ1 group. The level of miRNA589 was determined by realtime PCR. The expressions of ZO-1, vimentin, and E-cadherin in HPMCs were detected, respectively. Results. Decreased level of miRNA589 was obtained in either HPMCs of long-term CAPD patients or HMrSV5 cells treated with TGFβ1. In vitro, TGFβ1 led to upregulation 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 with TGFβ1. Overexpression of miRNA589 by transfection with pre-miRNA589 partially reversed these EMT changes. Conclusion. miRNA589 mediates TGFβ1 induced EMT in human peritoneal mesothelial cells.
Insights
MicroRNA 589 (miR589) plays a key role in preventing peritoneal fibrosis. Decreased miR589 levels promote epithelial-mesenchymal transition (EMT) in human peritoneal mesothelial cells, suggesting its therapeutic potential.
Area of Science:
- Molecular Biology
- Cell Biology
- Nephrology
Background:
- MicroRNAs (miRNAs) regulate gene expression and are implicated in epithelial-mesenchymal transition (EMT).
- The specific role of miRNAs in peritoneal fibrosis remains largely unexplored.
- Peritoneal fibrosis is a significant complication in patients undergoing continuous ambulatory peritoneal dialysis (CAPD).
Purpose of the Study:
- To investigate the regulatory role of microRNA 589 (miR589) in transforming growth factor beta 1 (TGFβ1)-induced EMT.
- To determine the expression levels of miR589 in human peritoneal mesothelial cells (HPMCs) from CAPD patients and in a cell line treated with TGFβ1.
- To assess the impact of miR589 overexpression on TGFβ1-induced EMT markers.
Main Methods:
- Real-time PCR was used to quantify miR589 levels in HPMCs and HMrSV5 cells.
- Human peritoneal mesothelial cells (HMrSV5) were treated with TGFβ1 to induce EMT.
- Cells were transfected with pre-miR-589 to study the effect of miR589 overexpression on EMT markers (ZO-1, vimentin, E-cadherin).
Main Results:
- miR589 levels were significantly decreased in HPMCs from CAPD patients and in HMrSV5 cells exposed to TGFβ1.
- TGFβ1 treatment induced EMT in HMrSV5 cells, characterized by increased vimentin and decreased ZO-1 and E-cadherin expression.
- Overexpression of miR589 partially reversed the TGFβ1-induced EMT, restoring normal expression of EMT markers.
Conclusions:
- miR589 acts as a crucial mediator in the TGFβ1-induced EMT process in human peritoneal mesothelial cells.
- Reduced miR589 levels are associated with peritoneal fibrosis development.
- miR589 represents a potential therapeutic target for mitigating peritoneal fibrosis.
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The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...