| First Author | Doverhag C | Year | 2010 |
| Journal | Neurobiol Dis | Volume | 38 |
| Issue | 1 | Pages | 36-46 |
| PubMed ID | 20053377 | Mgi Jnum | J:159938 |
| Mgi Id | MGI:4453085 | Doi | 10.1016/j.nbd.2009.12.024 |
| Citation | Doverhag C, et al. (2010) Galectin-3 contributes to neonatal hypoxic-ischemic brain injury. Neurobiol Dis 38(1):36-46 |
| abstractText | 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. |
