Title of article :
Identification of CD13+CD36+ cells as a common progenitor for erythroid and myeloid lineages in human bone marrow
Author/Authors :
Ling Chen، نويسنده , , Zhigang Gao، نويسنده , , Jianqiong Zhu، نويسنده , , Griffin P. Rodgers، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2007
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 14th 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.
Journal title :
Experimental Hematology
Journal title :
Experimental Hematology