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MicroRNAs contribute to induced pluripotent stem cell somatic donor memory
Marianna Vitaloni1, Julian Pulecio, Josipa Bilic
1From the Center for Regenerative Medicine in Barcelona, 08003 Barcelona, Spain and.
Abstract:
Induced pluripotent stem cells (iPSCs) maintain during the first few culture passages a set of epigenetic marks and metabolites characteristic of their somatic cell of origin, a concept defined as epigenetic donor memory. These residual somatic features are lost over time after extensive culture passaging. Therefore, epigenetic donor memory may be responsible for the higher differentiation efficiency toward the tissue of origin observed in low passage iPSCs versus high passage iPSC or iPSCs derived from a different tissue source. Remarkably, there are no studies on the relevance of microRNA (miRNA) memory following reprogramming, despite the established role of these molecules in the context of pluripotency and differentiation. Using hematopoietic progenitors cells as a model, we demonstrated that miRNAs play a central role in somatic memory retention in iPSCs. Moreover, the comparison of the miRNA expression profiles among iPSCs from different sources allowed for the detection of a set of candidate miRNAs responsible for the higher differentiation efficiency rates toward blood progenitors observed in low passage iPSCs. Combining bioinformatic predictive algorithms with biological target validation, we identified miR-155 as a key player for the in vitro differentiation of iPSC toward hematopoietic progenitors. In summary, this study reveals that during the initial passages following reprogramming, iPSCs maintained the expression of a miRNA set exclusive to the original somatic population. Hence the use of these miRNAs might hold a direct application toward our understanding of the differentiation process of iPSCs toward hematopoietic progenitor cells.
Insights
Induced pluripotent stem cells (iPSCs) retain microRNA (miRNA) signatures from their origin, influencing differentiation efficiency. This study identifies specific miRNAs, like miR-155, crucial for hematopoietic progenitor cell differentiation from iPSCs.
Area of Science:
- Stem cell biology
- Epigenetics
- Molecular biology
Background:
- Induced pluripotent stem cells (iPSCs) exhibit donor memory, retaining epigenetic and metabolic traits from their somatic origin.
- This memory is lost with extensive passaging, potentially affecting differentiation efficiency.
- The role of microRNA (miRNA) memory in iPSCs remains largely unexplored despite their importance in pluripotency and differentiation.
Purpose of the Study:
- To investigate the role of miRNA memory in maintaining somatic cell characteristics in iPSCs.
- To identify specific miRNAs responsible for enhanced differentiation efficiency towards the tissue of origin.
- To explore the potential application of miRNA memory in understanding iPSC differentiation.
Main Methods:
- Hematopoietic progenitor cells were used as a model system.
- miRNA expression profiles of iPSCs from different sources were compared.
- Bioinformatic predictive algorithms and biological target validation were employed.
- miR-155 was identified as a key miRNA through these analyses.
Main Results:
- miRNAs play a significant role in somatic memory retention in iPSCs.
- A set of candidate miRNAs was identified, correlating with higher differentiation efficiency towards blood progenitors in low-passage iPSCs.
- miR-155 was confirmed as a key regulator in the in vitro differentiation of iPSCs into hematopoietic progenitor cells.
- iPSCs maintain a unique miRNA expression profile from their original somatic cells in early passages.
Conclusions:
- This study establishes miRNA memory as a critical factor in iPSC behavior and differentiation.
- The findings highlight the potential of utilizing specific miRNAs, such as miR-155, to improve directed differentiation of iPSCs into specific cell types, particularly hematopoietic progenitors.
- Understanding miRNA memory offers new avenues for optimizing iPSC applications in regenerative medicine and disease modeling.
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