Galectin-1 stimulates monocyte chemotaxis via the p44/42 MAP kinase pathway and a pertussis toxin-sensitive pathway
Galectin-1 stimulates monocyte chemotaxis via the p44/42 MAP kinase pathway and a pertussis toxin-sensitive pathway
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DOI：
10.1093/glycob/cwp077
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发表时间：
2009-12-01
期刊：
影响因子：
4.3
通讯作者：
Stewart, Helen J. S.
中科院分区：
文献类型：
--
作者：
Malik, Reshad K. J.;Ghurye, Rohit R.;Stewart, Helen J. S.
Galectin-1是β-半乳糖苷结合蛋白家族的原型，参与了多种生物学过程。本文提供的数据表明，Galectin-1以剂量依赖的方式刺激单核细胞迁移，但对巨噬细胞不趋化。Galectin-1诱导的单核细胞趋化可被乳糖阻断，并被抗Galectin-1抗体抑制，但不被非特异性抗体所抑制。此外，MEK抑制剂以一种快速、时间依赖的方式显著抑制Galectin-1介导的单核细胞迁移，提示MAPK通路参与Galectin-1。迁移也几乎完全被百日咳毒素阻断，这意味着G蛋白参与了Galectin-1诱导的趋化作用。这些结果表明Galectin-1在单核细胞趋化中的作用，这与Galectin-3的不同之处在于巨噬细胞是无反应的。此外，我们的观察表明，Galectin-1可能参与体内炎症部位的化学吸引，并可能参与动脉粥样硬化等疾病过程。
Galectin-1, the prototype of a family of beta-galactoside-binding proteins, has been implicated in a wide variety of biological processes. Data presented herein show that galectin-1 stimulates monocyte migration in a dose-dependent manner but is not chemotactic for macrophages. Galectin-1-induced monocyte chemotaxis is blocked by lactose and inhibited by an anti-galectin-1 antibody but not by nonspecific antibodies. Furthermore, galectin-1-mediated monocyte migration was significantly inhibited by MEK inhibitors in a rapid, time-dependent manner suggesting that MAP kinase pathways are involved in galectin-1. Migration was also almost completely blocked by pertussis toxin implying G-protein involvement in the galectin-1-induced chemotaxis. These results demonstrate a role for galectin-1 in monocyte chemotaxis which differs from galectin-3 in that macrophages are nonresponsive. Furthermore, our observations suggest that galectin-1 may be involved in chemoattraction at sites of inflammation in vivo and may contribute to disease processes such as atherosclerosis.