Galectin-1 promotes Schwann cell migration
Arata Segawa, Hiroko Inoue, Waseda University
Galectins, a family of the β-galactoside-binding lectins, have numerous functions. Galectin-1 (Gal-1), the prototype of galectins, regulates apoptosis, cell proliferation, and cell differentiation. It exists in both reduced and oxidized states, and oxidized Gal-1 (Gal-1/Ox) plays various important roles in the regeneration of the peripheral nervous system after injury. On the other hand, whether reduced Gal-1 (Gal-1/Re) affects regeneration is unknown. An important step in the regeneration of axons is the recruitment of Schwann cells to the site of injury through chemotactic molecules. In this study, we investigated the effects of Gal-1/Re on Schwann cell migration after injury using the wound healing assay. When RT4-D6P2T Schwann cells were exposed to Gal-1/Re, cell migration increased at 5 ng/ml and decreased gradually in a dose-dependent manner. Motility was inhibited by lactose, suggesting that Gal-1/Re bound to the receptor on the RT4-D6P2T Schwann cell membrane, and enhanced cell migration. Gal-1 stimulates squamous cell carcinoma cell migration by activating c-Jun N-terminal kinase (JNK). Therefore, we examined the effect of SP600125, a specific inhibitor of JNK, and found that Gal/Re-induced Schwann cell migration was mediated by JNK. Although cell migration activated by Gal-1/Ox was mediated by the MEK/ERK1/2 pathway, PD98059, a specific inhibitor of MEK did not affect Gal-1/Re-induced cell migration. These results suggested that Gal-1/Re stimulated the migration of RT4-D6P2T Schwann cells via JNK.