Rao Mahil, Supakorndej Teerawit, Schmidt Amy P, Link Daniel C
Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA.
Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA.
Exp Hematol. 2015 Feb;43(2):110-4.e1-2. doi: 10.1016/j.exphem.2014.10.012. Epub 2014 Nov 1.
The contribution of osteoclasts to hematopoietic stem/progenitor cell (HSPC) retention in the bone marrow is controversial. Studies of HSPC trafficking in osteoclast-deficient mice are limited by osteopetrosis. Here, we employed two non-osteopetrotic mouse models to assess the contribution of osteoclasts to basal and granulocyte colony-stimulating factor (G-CSF)-induced HSPC mobilization. We generated Rank(-/-) fetal liver chimeras using Csf3r(-/-) recipients to produce mice lacking G-CSF receptor expression in osteoclasts. Basal and G-CSF-induced HSPC mobilization was normal in these chimeras. We next acutely depleted osteoclasts in wild-type mice using the RANK ligand inhibitor osteoprotegerin. Marked suppression of osteoclasts was observed after a single injection of osteoprotegerin-Fc. Basal and G-CSF-induced HSPC mobilization in osteoprotegerin-Fc-treated mice was comparable to that in control mice. Together, these data indicate that osteoclasts are not required for the efficient retention of HSPCs in the bone marrow and are dispensable for HSPC mobilization by G-CSF.
破骨细胞对造血干细胞/祖细胞(HSPC)保留在骨髓中的作用存在争议。在破骨细胞缺陷小鼠中对HSPC迁移的研究受到骨质石化的限制。在此,我们采用两种非骨质石化小鼠模型来评估破骨细胞对基础和粒细胞集落刺激因子(G-CSF)诱导的HSPC动员的作用。我们使用Csf3r(-/-)受体生成Rank(-/-)胎肝嵌合体,以产生在破骨细胞中缺乏G-CSF受体表达的小鼠。这些嵌合体中的基础和G-CSF诱导的HSPC动员是正常的。接下来,我们使用RANK配体抑制剂骨保护素在野生型小鼠中急性清除破骨细胞。单次注射骨保护素-Fc后观察到破骨细胞受到明显抑制。骨保护素-Fc处理的小鼠中基础和G-CSF诱导的HSPC动员与对照小鼠相当。总之,这些数据表明破骨细胞对于HSPC在骨髓中的有效保留不是必需的,并且对于G-CSF诱导的HSPC动员是可有可无的。