Figure 7
Figure 7. Schematic illustration of the proposed model for the epigenetic plasticity of hematopoietic cells. Undifferentiated hematopoietic cells (A) have dynamic chromatin and display permissiveness to changes in chromatin structures and multilineage differentiation potential. In the undifferentiated state, epigenetic treatment (B) that opens chromatin structures (AZA/TSA) enhances HSC self-renewal when other extrinsic signals are present. In contrast, differentiated cells (C) have stable chromatin and are resistant to epigenetic changes. Epigenetic treatment with AZA/TSA leads to a partial dedifferentiation toward more immature cell phenotypes (D), although most of differentiated cells undergo extensive apoptosis. Thus, epigenetic plasticity correlates to the level of undifferentiation of hematopoietic cells.

Schematic illustration of the proposed model for the epigenetic plasticity of hematopoietic cells. Undifferentiated hematopoietic cells (A) have dynamic chromatin and display permissiveness to changes in chromatin structures and multilineage differentiation potential. In the undifferentiated state, epigenetic treatment (B) that opens chromatin structures (AZA/TSA) enhances HSC self-renewal when other extrinsic signals are present. In contrast, differentiated cells (C) have stable chromatin and are resistant to epigenetic changes. Epigenetic treatment with AZA/TSA leads to a partial dedifferentiation toward more immature cell phenotypes (D), although most of differentiated cells undergo extensive apoptosis. Thus, epigenetic plasticity correlates to the level of undifferentiation of hematopoietic cells.

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