期刊
BLOOD
卷 123, 期 7, 页码 992-1001出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2013-04-498469
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资金
- National Institutes of Health (National Cancer Institute) [1R01CA172268]
- Department of Defense [W81XWH-10-1-0429]
- Cancer Prevention Research Institute of Texas [RP100402]
- National Natural Science Foundation of China [21328503]
- Program for Professor of Special Appointment (Eastern Scholar), Shanghai, China
- Robert A. Welch Foundation [I-1834]
- Gabrielle's Angel Foundation
How stem cells interact with the microenvironment to regulate their cell fates and metabolismis largely unknown. Here we demonstrated that the deletion of the cytoskeleton modulating protein profilin 1 (pfn1) in hematopoietic stem cell (HSCs) led to bone marrow failure, loss of quiescence, and mobilization and apoptosis of HSCs in vivo. A switch from glycolysis to mitochondrial respiration with increased reactive oxygen species (ROS) level was also observed in HSCs on pfn1 deletion. Importantly, treatment of pfn1-deficient mice with the antioxidant N-acetyl-L-cysteine reversed the ROS level and loss of quiescence of HSCs, suggesting that the metabolism is mechanistically linked to the cell cycle quiescence of stem cells. The actin-binding and proline-binding activities of pfn1 are required for its function in HSCs. Our study provided evidence that pfn1 at least partially acts through the axis of pfn1/G alpha 13/EGR1 to regulate stem cell retention and metabolism in the bone marrow.
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