Dual function of galectin-1 in microglial activation of the brain

Abstract

Abstract Galectins-1, one of the β-galactosides-binding soluble lectin family, exert various roles in immune responses, and have been reported to be closely linked with several inflammation-associated diseases including cancer. However, their roles and underlying mechanisms remain largely unknown in the brain inflammation. In this study, we provide that galectin-1 could act as a regulatory molecule in the brain pathological conditions. Galectin-1 expression is markedly induced in IFN-g-treated microglial cells. In intracranial brain tumor model, we show that expression level of galectin-1 is significantly higher in B35 brain tumor cells and tumor neighboring microglial cells. Treatment of exogenous galectin-1 changes morphology of microglia, and induces expression of ICAM-1, adhesion molecule. In addition, galectin-1 triggers production of both pro-inflammatory mediators and anti-inflammatory mediators. Galectin-1-treated microglial cells activate lymphocytes. These findings indicate that galectin-1 involved in regulation of M1 and M2 phenotype of microglial cells. Therefore, we strongly suggest that galectin-1 may be dual roles in microglial activation of the brain pathophysiological environment.