Galectin-3 contributes to neonatal hypoxic-ischemic brain injury.

Christina Doverhag (1) , Maj Hedtjärn (1) , Françoise Poirier (2) , Carina Mallard (1) , Henrik Hagberg (1) , Anna Karlsson (3) , Karin Sävman (1)

1 Perinatal Center
2 IJM (UMR_7592) - Institut Jacques Monod
3 Department of Rheumatology & Inflammation Research

Inflammation induced by hypoxia-ischemia (HI) contributes to the development of injury in the newborn brain. In this study, we investigated the role of galectin-3, a novel inflammatory mediator, in the inflammatory response and development of brain injury in a mouse model for neonatal HI. Galectin-3 gene and protein expression was increased after injury and galectin-3 was located in activated microglia/macrophages. Galectin-3-deficient mice (gal3-/-) were protected from injury particularly in hippocampus and striatum. Microglia accumulation was increased in the gal3-/- mice but accompanied by decreased levels of total matrix metalloproteinase (MMP)-9 and nitrotyrosine. The protection and increase in microglial infiltration was more pronounced in male gal3-/- mice. Trophic factors and apoptotic markers did not significantly differ between groups. In conclusion, galectin-3 contributes to neonatal HI injury particularly in male mice. Our results indicate that galectin-3 exerts its effect by modulating the inflammatory response.

Domaines: Neurobiologie; Médecine humaine et pathologie

Christina Doverhag, Maj Hedtjärn, Françoise Poirier, Carina Mallard, Henrik Hagberg, et al.. Galectin-3 contributes to neonatal hypoxic-ischemic brain injury.. Neurobiology of Disease, 2010, 38 (1), pp.36-46. ⟨10.1016/j.nbd.2009.12.024⟩. ⟨hal-00488063⟩