Stromal derived factor-1-induced chemokinesis of cord blood CD34+ cells (long-term culture-initiating cells) through endothelial cells is mediated by E-selectin
Stromal derived factor-1-induced chemokinesis of cord blood CD34+ cells (long-term culture-initiating cells) through endothelial cells is mediated by E-selectin
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DOI：
10.1182/blood.v94.12.4011.424k10_4011_4019
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发表时间：
1999-12-15
期刊：
影响因子：
20.3
通讯作者：
Rafii, S
中科院分区：
文献类型：
--
作者：
Naiyer, AJ;Jo, DY;Rafii, S
造血干细胞归巢至骨髓 (BM) 涉及与 BM 内皮 (BMEC) 上表达的粘附分子和趋化因子基质衍生因子 1 (SDF-1) 的连续相互作用。然而，粘附分子调节 SDF-1 诱导的跨内皮迁移过程的机制尚不清楚。 E-选择素是一种内皮特异性选择素，由 BMEC 在体内组成型表达。因此，我们推测E-选择素可能介导SDF-1诱导的CD34+细胞的跨内皮迁移。我们发现CD34(+)细胞同时表达E-选择素配体和岩藻糖基转移酶-VII (FucT-VII)。可溶性 E-选择素-IgG 嵌合体与 75% +/- 10% 的 CD34(+) 细胞紧密结合，这些细胞主要由祖细胞和具有长期培养起始细胞 (LTC-IC) 潜力的细胞组成。为了评估E-选择素在跨内皮迁移系统中介导CD34(+)细胞迁移的功能能力，将CD34(+)细胞置于涂有白介素-1β激活的BMEC的Transwell平板上。在不存在SDF-1的情况下，7.0%+/-1.4%的CD34(+)细胞和14.1%+/-2.2%的LTC-IC自发迁移，SDF-1诱导另外23.0%+/-4.4%的CD34(+)细胞和17.6%+/-3.6%的LTC-IC迁移。阻断MoAb对E-选择素的抑制可抑制SDF-1诱导的CD34(+)细胞迁移42.0%+/-2.5%和LTC-IC迁移90.9%+/-16.6%。为了明确体内BMEC组成型表达E-选择素的机制，我们发现血管内皮生长因子(VEGF(165))诱导培养的内皮细胞表达E-选择素，VEGF刺激的内皮细胞支持CD34(+)细胞跨内皮迁移，而MoAb可以阻断CD34(+)细胞向E-选择素的迁移。 具有 LTC-IC 潜力的 CD34(+) 细胞亚群部分是由与 E-选择素和 SDF-1 的顺序相互作用决定的。 (C) 1999 年，美国血液学会。
Homing of hematopoietic stem cells to the bone marrow (BM) involves sequential interaction with adhesion molecules expressed on BM endothelium (BMEC) and chemokine stromal derived factor-1 (SDF-1). However, the mechanism whereby adhesion molecules regulate the SDF-1-induced transendothelial migration process is not known. E-selectin is an endothelial-specific selectin that is constitutively expressed by the BMEC in vivo. Hence, we hypothesized that E-selectin may mediate SDF-1-induced transendothelial migration of CD34(+) cells. We show that CD34(+) cells express both E-selectin ligand and fucosyltransferase-VII (FucT-VII). Soluble E-selectin-IgG chimera binds avidly to 75% +/- 10% of CD34(+) cells composed mostly of progenitors and cells with long-term culture-initiating cell (LTC-IC) potential. To assess the functional capacity of E-selectin to mediate CD34(+) cell migration in a transendothelial migration system, CD34(+) cells were placed on transwell plates coated with interleukin-1 beta-activated BMEC. In the absence of SDF-1, there was spontaneous migration of 7.0% +/- 1.4% of CD34(+) cells and 14.1% +/- 2.2% of LTC-IC, SDF-1 induced migration of an additional 23.0% +/- 4.4% of CD34(+) cells and 17.6% +/- 3.6% of LTC-IC. Blocking MoAb to E-selectin inhibited SDF-1-induced migration of CD34(+) cells by 42.0% +/- 2.5% and LTC-IC by 90.9% +/- 16.6%. To define the mechanism of constitutive expression of E-selectin by the BMEC in vivo, we have found that vascular endothelial growth factor (VEGF(165)) induces E-selectin expression by cultured endothelial cells, VEGF-stimulated endothelial cells support transendothelial migration of CD34(+) cells that could be blocked by MoAb to E-selectin, These results suggest that trafficking of subsets of CD34(+) cells with LTC-IC potential is determined in part by sequential interactions with E-selectin and SDF-1. (C) 1999 by The American Society of Hematology.