Repair of the damaged trophoblast cells through CD44-mediated signaling

研究CD44v3和肝素/硫酸肝素(HS)信号在滋养层细胞迁移过程中的作用。我们评价了肝素/HS/CD44v3介导的过程在TCL-1细胞划痕愈合过程中的作用。体外划痕伤口愈合试验显示，与对照组相比，在肝素存在的情况下，滋养层细胞以剂量依赖的方式迁移。相反，在类似的划痕实验中，抗CD44功能阻断抗体和CD44siRNA在肝素存在的情况下抑制滋养层细胞的迁移。肝素处理和体外划痕损伤均可诱导p21激活蛋白1(PAK1)的磷酸化，而抗CD44v3抗体则抑制肝素诱导的PAK1的磷酸化。这些结果表明，在缺乏生长因子网络的情况下，肝素/硫酸肝素/CD44v3介导的信号通过滋养层细胞的迁移促进了受损滋养层的直接修复。

The function of CD44v3 and heparin/heparan sulphate (HS) signaling was investigated during trophoblast cell migration. We evaluated the effect of heparin/ HS/CD44v3-mediated processes during scratch wound closure in TCL-1 cells. An in vitro scratch wound healing assay showed enhanced migration of trophoblast cells in a dose-dependent manner in the presence of heparin compared with controls. Conversely, an anti-CD44 function blocking antibody and CD44siRNA suppressed the migration of trophoblast cells in the presence of heparin in a similar scratch assay. Both heparin treatment and in vitro scratch wounding induced the phosphorylation of p21-activated kinase 1 (PAK1), while the anti-CD44v3 antibody suppressed the heparin-induced phosphorylation of PAK1. These results indicate that heparin/heparan sulphate/CD44v3-mediated signaling, in the absence of growth factor networks, enhances the direct repair of the damaged trophoblast layer through the migration of trophoblast cells.