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Updated: Jun 1, 2026

Identifying Bone Marrow Microenvironmental Populations in Myelodysplastic Syndrome and Acute Myeloid Leukemia
Published on: November 10, 2023
Stromal-derived factor-1 deficiency in the bone marrow of acute myeloid leukemia
Jian Ge1, Ruiqin Hou1, Quanhua Liu1
1Peking University Institute of Hematology, Peking University People's Hospital, 11 Xizhimen South Street, Xicheng District, Beijing, 100044, People's Republic of China.
Chemokine stromal-derived factor-1 (SDF-1) and its receptor CXCR4 have been shown to play an important role in the migration and homing of the transplanted hematopoietic stem cells (HSCs). Mesenchymal stem cells (MSCs) express these molecules. This study is to test the hypothesis that acute myeloid leukemia (AML) alters the expression of SDF-1/CXCR4 in human bone marrow MSCs. Expression of both CXCR4 and SDF-1 was found to be increased, but excessively retained, in the MSCs in AML. In contrast, the SDF-1 level in bone marrow plasma and supernatant of cultured MSCs from AML patients were reduced, while the SDF-1 was able to efficiently induce a dose-dependent migration of MSCs in vitro. Our results demonstrate that altered expression and distribution of SDF-1/CXCR4 in MSCs may contribute to SDF-1 deficiency in the plasma of AML patients. The migration of MSCs may be negatively affected by the SDF-1 deficiency.
Chemokine stromal-derived factor-1 (SDF-1) and its receptor CXCR4 have been shown to play an important role in the migration and homing of the transplanted hematopoietic stem cells (HSCs). Mesenchymal stem cells (MSCs) express these molecules. This study is to test the hypothesis that acute myeloid leukemia (AML) alters the expression of SDF-1/CXCR4 in human bone marrow MSCs. Expression of both CXCR4 and SDF-1 was found to be increased, but excessively retained, in the MSCs in AML. In contrast, the SDF-1 level in bone marrow plasma and supernatant of cultured MSCs from AML patients were reduced, while the SDF-1 was able to efficiently induce a dose-dependent migration of MSCs in vitro. Our results demonstrate that altered expression and distribution of SDF-1/CXCR4 in MSCs may contribute to SDF-1 deficiency in the plasma of AML patients. The migration of MSCs may be negatively affected by the SDF-1 deficiency.
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