Ling Chen1, Zhigang Gao, Jianqiong Zhu, Griffin P Rodgers. 1. Molecular and Clinical Hematology Branch (MCHB), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Abstract
OBJECTIVE: To identify bipotential precursor cells of erythroid and myeloid development in human bone marrow. MATERIALS AND 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. 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.
OBJECTIVE: To identify bipotential precursor cells of erythroid and myeloid development in human bone marrow. MATERIALS AND 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. 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.
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