The role of selenite on microglial migration.
Oxidative brain damage, such as excitotoxicity and stroke, leads to primary neuronal destruction. The primary damage is further potentiated by macrophages and microglial cells, which are attracted and invade into the zone of damage resulting in secondary neuronal death. Since the essential trace element selenium has anti-inflammatory properties, we analyzed the effects of selenium on these inflammatory cells. Here, we show that the essential trace element selenium abrogates the stress-induced migration of microglial cells. Thus, the antimigratory effects of selenium may attenuate the secondary cell death cascade by preventing microglial invasion.
Dalla Puppa
Lisa
L
Hahn-Meitner-Institute, Department of Molecular Trace Element Research in the Life Sciences, Glienicker Str. 100, 14109 Berlin, Germany. dallapuppa@web.de
Savaskan
Nicolai E
NE
Bräuer
Anja U
AU
Behne
Dietrich
D
Kyriakopoulos
Antonios
A
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D040881:CD11a Antigen / Q000096:biosynthesis; D002460:Cell Line; D002465:Cell Movement; D002469:Cell Separation; D005786:Gene Expression Regulation; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007249:Inflammation; D008264:Macrophages / Q000187:drug effects*; D051379:Mice; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D009474:Neurons / Q000378:metabolism; D012643:Selenium / Q000494:pharmacology*; D018038:Sodium Selenite / Q000494:pharmacology*
D000893:Anti-Inflammatory Agents; D040881:CD11a Antigen; D006861:Hydrogen Peroxide; D012643:Selenium; D018038:Sodium Selenite