PT - JOURNAL ARTICLE AU - Claude, Janine AU - Linnartz-Gerlach, Bettina AU - Kudin, Alexei P. AU - Kunz, Wolfram S. AU - Neumann, Harald TI - Microglial CD33-Related Siglec-E Inhibits Neurotoxicity by Preventing the Phagocytosis-Associated Oxidative Burst AID - 10.1523/JNEUROSCI.2211-13.2013 DP - 2013 Nov 13 TA - The Journal of Neuroscience PG - 18270--18276 VI - 33 IP - 46 4099 - http://www.jneurosci.org/content/33/46/18270.short 4100 - http://www.jneurosci.org/content/33/46/18270.full SO - J. Neurosci.2013 Nov 13; 33 AB - Sialic acid-binding Ig-like lectins (Siglecs) are members of the Ig superfamily that recognize sialic acid residues of glycoproteins. Siglec-E is a mouse CD33-related Siglec that preferentially binds to sialic acid residues of the cellular glycocalyx. Here, we demonstrate gene transcription and protein expression of Siglec-E by cultured mouse microglia. Siglec-E on microglia inhibited phagocytosis of neural debris and prevented the production of superoxide radicals induced by challenge with neural debris. Soluble extracellular Siglec-E receptor protein bound to the neural glycocalyx. Coculture of mouse microglia and neurons demonstrated a neuroprotective effect of microglial Siglec-E that was dependent on neuronal sialic acid residues. Increased neurotoxicity of microglia after knockdown of Siglece mRNA was neutralized by the reactive oxygen species scavenger Trolox. Data suggest that Siglec-E recognizes the intact neuronal glycocalyx and has neuroprotective function by preventing phagocytosis and the associated oxidative burst.