Engulfment of Toxic Amyloid β-protein in Neurons and Astrocytes Mediated by MEGF10

Neuroscience. 2020 Sep 1:443:1-7. doi: 10.1016/j.neuroscience.2020.07.016. Epub 2020 Jul 16.

Abstract

Amyloid-β proteins (A β), including Aβ42 and A β 43, are known pathogenesis factors of Alzheimer's disease (AD). Unwanted substances in the brain, including A β, are generally removed by microglia, astrocytes, or neurons via a phagocytosis receptor. We observed that neurons and astrocytes engulfed A β 42 and A β 43, which are more neurotoxic than A β 40. We previously showed that multiple-EGF like domains 10 (MEGF10) plays an important role in apoptotic cell elimination and is expressed in mammalian neurons and astrocytes. Therefore, we assessed whether MEGF10 is involved in A β42 and A β43 engulfment in MEGF10-expressing neurons and astrocytes. We found that MEGF10-expressing astrocytes and neurons engulfed A β42 and A β43 but not A β40. Furthermore, incubation of the neurons and astrocytes with A β42 and A β43a ugmented MEGF10 phosphorylation; however, incubation with A β40 did not have this augmenting effect. Our findings suggest that MEGF10 plays a phagocytosis receptor function for A β42 and A β43 in neurons and astrocytes.

Keywords: MEGF10; amyloid-β protein; draper; phagocytosis receptor; phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease*
  • Amyloid beta-Peptides* / toxicity
  • Animals
  • Astrocytes
  • Membrane Proteins
  • Neurons

Substances

  • Amyloid beta-Peptides
  • Membrane Proteins