Rapid hematopoietic progenitor mobilization by sulfated colominic acid
Rapid hematopoietic progenitor mobilization by sulfated colominic acid
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DOI：
10.1016/j.bbrc.2007.02.069
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发表时间：
2007-04-20
影响因子：
3.1
通讯作者：
Katayama, Yoshio
中科院分区：
文献类型：
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作者：
Kubonishi, Shiro;Kikuchi, Tomoko;Katayama, Yoshio
造血祖细胞（HPCs）可以通过G-CSF从骨髓（BM）动员到血液中。在这一过程中，CXCR4和CD26发挥了关键作用。硫酸二酚酸（SCA）抑制HIV进入，这一步骤需要CXCR4和CD26作为共受体。因此，我们假设SCA会调节HPC贩运。我们首先发现SCA通过不依赖cd26的机制快速调动HPCs。SCA显著增强了体外祖细胞向趋化因子SDF-1的迁移，并被CXCR4抑制完全消除。这可能源于与SDF-1相互作用后CXCR4下调受到抑制。注射SCA后血清SDF-1水平升高，而BM和bone没有变化。这些结果表明SCA通过调节CXCR4功能诱导HPC动员，从而导致循环中SDF-1的增加。此外，我们证实了G-CSF在动员中的加性作用。SCA可能在临床动员中发挥作用。(c) 2007爱思唯尔公司版权所有。
Hematopoietic progenitor cells (HPCs) can be mobilized from bone marrow (BM) to the blood by G-CSF. In this process, CXCR4 and CD26 play critical roles. Sulfated colominic acid (SCA) inhibits HIV entry, the step which requires CXCR4 and CD26 as co-receptors. Thus, we hypothesized that SCA would modulate HPC trafficking. We first found that SCA mobilized HPCs rapidly via CD26-independent mechanism. In vitro progenitor migration toward chemokine SDF-1 was significantly enhanced by SCA, and it was completely abrogated by CXCR4 inhibition. This likely originated from the inhibition of CXCR4 down-regulation after interaction with SDF-1. Serum SDF-1 level increased after SCA injection, whereas no change was observed in BM and bone. These results suggest that SCA induces HPC mobilization by modulating CXCR4 function resulting in attraction toward increased SDF-1 in the circulation. Furthermore, we confirmed an additive effect with G-CSF in mobilization. SCA may provide an efficacy in clinical mobilization. (c) 2007 Elsevier Inc. All rights reserved.