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Updated: Jan 22, 2026
10:37
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
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UA promotes epithelial‑mesenchymal transition in peritoneal mesothelial cells
Chao-Yang Duan1, Jin Han1, Chong-Yu Zhang2
1Department of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Molecular Medicine Reports
|July 20, 2019
Summary
High uric acid (UA) levels promote peritoneal fibrosis by inducing epithelial-mesenchymal transition (EMT) in mesothelial cells. Lowering blood UA may inhibit peritoneal fibrosis development and progression.
Area of Science:
- Nephrology
- Cell Biology
- Pathology
Background:
- Peritoneal fibrosis limits long-term peritoneal dialysis.
- Epithelial-mesenchymal transition (EMT) is implicated in peritoneal injury but mechanisms are unclear.
Purpose of the Study:
- Investigate uric acid (UA)-induced EMT in peritoneal mesothelial cells.
- Elucidate the molecular pathways involved in UA-mediated EMT.
Main Methods:
- Western blot and immunofluorescence staining to assess protein expression.
- Reverse transcription semi-quantitative polymerase chain reaction to analyze gene expression.
- Stimulation of peritoneal mesothelial cells with UA.
Main Results:
- UA induced EMT in peritoneal mesothelial cells, decreasing epithelial marker (E-cadherin) and increasing mesenchymal markers (α-smooth muscle actin, vimentin).
- UA promoted EMT via TGF-β1/Smad3 and p38/MAPK pathways.
- UA contributes to peritoneal chronic disease and fibrosis.
Conclusions:
- UA is a key factor in promoting EMT and peritoneal fibrosis.
- Blood UA levels correlate with EMT development.
- Lowering blood UA may be a therapeutic strategy against peritoneal fibrosis.
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