RT Journal Article
SR Electronic
T1 Microglial CD33-Related Siglec-E Inhibits Neurotoxicity by Preventing the Phagocytosis-Associated Oxidative Burst
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 18270
OP 18276
DO 10.1523/JNEUROSCI.2211-13.2013
VO 33
IS 46
A1 Claude, Janine
A1 Linnartz-Gerlach, Bettina
A1 Kudin, Alexei P.
A1 Kunz, Wolfram S.
A1 Neumann, Harald
YR 2013
UL http://www.jneurosci.org/content/33/46/18270.abstract
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.