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

Neuroscience
Yu FujitaHiroto Komano

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.

References

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Sep 11, 2010·FEBS Letters·Thoudam Debraj SinghIn-San Kim
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Mar 10, 2017·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Chia-Chen LiuGuojun Bu
May 21, 2017·Neuroscience Letters·Yu FujitaHiroto Komano

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Citations

Jun 3, 2021·Cells·Rena KonoRyuta Koyama
Oct 7, 2021·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Johanna TüshausStefan F Lichtenthaler

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