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Updated: Feb 16, 2026
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition
Anna Sola1, Laura Saenz Del Burgo1,2, Jesús Ciriza1,2
1a Biomedical Research Networking Center in Bioengineering , Biomaterials and Nanomedicine (CIBER-BBN) , Barcelona , Spain.
Abstract:
Epithelial to mesenchymal transition (EMT) has emerged as a key process in the development of renal fibrosis. In fact, EMT-derived fibroblasts contribute to the progression of chronic renal disease. In addition, anti-inflammatory M2 macrophages have exhibited a great influence on renal fibrosis. However, because of the high impact that the inputs of different environmental cytokines have on their phenotype, macrophages can easily lose this property. We aim to known if microencapsulated macrophages on M2-inducing alginate matrices could preserve macrophage phenotype and thus release factors able to act on epithelial cells to prevent the epithelial differentiation towards mesenchymal cells. We reproduced an in vitro model of EMT by treating adipose-derived stem cells with all-trans retinoic acid (ATRA) and induced their transformation toward epithelia. Dedifferentiation of epithelial cells into a mesenchymal phenotype occurred when ATRA was retired, thus simulating EMT. Results indicate that induction of M2 phenotype by IL-10 addition in the alginate matrix produces anti-inflammatory cytokines and increases the metabolic activity and the viability of the encapsulated macrophages. The released conditioned medium modulates EMT and maintains healthy epithelial phenotype. This could be used for in vivo cell transplantation, or alternatively as an external releaser able to prevent epithelial to mesenchymal transformation for future anti-fibrotic therapies.
Insights
Microencapsulated M2 macrophages in alginate matrices preserve their anti-inflammatory properties. This approach prevents epithelial to mesenchymal transition (EMT), offering a novel strategy for anti-fibrotic therapies.
Area of Science:
- Biomedical Engineering
- Cell Biology
- Regenerative Medicine
Background:
- Epithelial to mesenchymal transition (EMT) drives renal fibrosis and chronic kidney disease progression.
- M2 macrophages possess anti-fibrotic properties but are susceptible to phenotype changes.
- Maintaining M2 macrophage phenotype is crucial for therapeutic efficacy.
Purpose of the Study:
- To investigate if microencapsulated M2 macrophages in alginate matrices can preserve their phenotype.
- To determine if these encapsulated macrophages can release factors to inhibit EMT.
- To explore potential anti-fibrotic therapeutic applications.
Main Methods:
- Developed an in vitro EMT model using adipose-derived stem cells and all-trans retinoic acid (ATRA).
- Encapsulated macrophages in M2-inducing alginate matrices with IL-10.
- Analyzed macrophage phenotype, cytokine release, and conditioned medium effects on epithelial cells.
Main Results:
- IL-10 induction successfully generated M2 macrophages within alginate matrices.
- Encapsulated M2 macrophages exhibited enhanced viability and metabolic activity.
- Conditioned medium from encapsulated macrophages modulated EMT and maintained epithelial cell phenotype.
Conclusions:
- Microencapsulation in alginate matrices effectively preserves M2 macrophage phenotype and function.
- This strategy shows promise for preventing epithelial to mesenchymal transition.
- Potential applications include cell transplantation and cell-free anti-fibrotic therapies.
