Conclusions
The present data identify some CD13+CD36+ cells as bipotential precursors of erythroid and myeloid commitment in normal hematopoiesis. They provide a physiological explanation for the cell identification of myeloid and erythroid lineages observed in hematopoietic diseases. This unique fraction of CD13+CD36+ cells may be useful for further studies on regulating erythroid and myeloid differentiation during normal and malignant hematopoiesis.
Methods
Cells coexpressing CD13 and CD36 (CD13+CD36+) were investigated by analyzing cell-surface marker expression during erythroid development (induced with a combination of cytokines plus erythropoietin), or myeloid development (induced with the same cocktail of cytokines plus granulocyte colony-stimulating factor of bone marrow-derived CD133 cells in liquid cultures. CD13+CD36+ subsets were also isolated on the 14(th) day of cultures and further evaluated for their hematopoietic clonogenic capacity in methylcellulose.
Objective
To identify bipotential precursor cells of erythroid and myeloid development in human bone marrow. Materials and
Results
Colony-forming analysis of sorted CD13+CD36+ cells of committed erythroid and myeloid lineages demonstrated that these cells were able to generate erythroid, granulocyte, and mixed erythroid-granulocyte colonies. In contrast, CD13+CD36- or CD13-CD36+ cells exclusively committed to granulocyte/monocyte or erythroid colonies, respectively, but failed to form mixed erythroid-granulocyte colonies; no colonies were detected in CD13-CD36- cells with lineage-supporting cytokines. In addition, our data confirmed that erythropoietin induced both erythroid and myeloid commitment, while granulocyte colony-stimulating factor only supported the differentiation of the myeloid lineage. Conclusions: The present data identify some CD13+CD36+ cells as bipotential precursors of erythroid and myeloid commitment in normal hematopoiesis. They provide a physiological explanation for the cell identification of myeloid and erythroid lineages observed in hematopoietic diseases. This unique fraction of CD13+CD36+ cells may be useful for further studies on regulating erythroid and myeloid differentiation during normal and malignant hematopoiesis.
