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Updated: Feb 10, 2026
06:02
Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition
Published on: June 10, 2016
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Functional molecules in mesothelial-to-mesenchymal transition revealed by transcriptome analyses.
Sara Namvar1,2, Adrian S Woolf1,2,3, Leo Ah Zeef4
1Division of Cell Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
The Journal of Pathology
|May 19, 2018
Summary
Defining the molecular signature of mesothelial-to-mesenchymal transition (MMT) revealed that bone morphogenetic protein 4 (BMP4) and insulin-like growth factor-binding protein 4 (IGFBP4) can reduce MMT, offering potential therapeutic strategies for peritoneal fibrosis.
Area of Science:
- Cell Biology
- Pathology
- Biochemistry
Background:
- Peritoneal fibrosis is a significant complication following abdominal surgery or peritoneal dialysis, often leading to treatment failure.
- Activated myofibroblasts, partly derived from mesothelial-to-mesenchymal transition (MMT), drive fibrosis.
- Understanding the molecular mechanisms of MMT is crucial for developing therapeutic interventions.
Purpose of the Study:
- To define the molecular signature of MMT.
- To identify potential therapeutic targets to inhibit MMT and subsequent peritoneal fibrosis.
- To investigate the role of specific signaling pathways in MMT.
Main Methods:
- Purification of rat peritoneal mesothelial cells using HBME1 antibody and streptavidin nanobead technology.
- Induction of MMT using transforming growth factor-β1 (TGF-β1) and subsequent RNA sequencing.
- Treatment with recombinant bone morphogenetic protein 4 (BMP4) or insulin-like growth factor-binding protein 4 (IGFBP4) to assess MMT inhibition.
- Immunohistochemical analysis of peritoneal tissue from patients and a mouse model.
Main Results:
- MMT was associated with altered expression of genes in insulin-like growth factor (IGF) and bone morphogenetic protein (BMP) signaling pathways.
- BMP4 and IGFBP4 treatments ameliorated TGF-β1-induced MMT in cultured cells, preserving epithelial phenotypes and reducing migration.
- Reduced expression of IGFBP4 and BMP4 was observed in peritoneal tissue from dialysis patients and in a mouse model of peritoneal injury.
Conclusions:
- A distinct molecular signature for MMT has been identified.
- BMP4 and potentially IGFBP4 show therapeutic promise for reducing MMT and mitigating peritoneal fibrosis.
- Targeting these pathways could offer new strategies for managing peritoneal fibrosis complications.
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