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Amyloid-beta-induced astrocytic phagocytosis is mediated by CD36, CD47 and RAGE.

Authors: Jones, RS  Minogue, AM  Connor, TJ  Lynch, MA 
Citation: Jones RS, etal., J Neuroimmune Pharmacol. 2013 Mar;8(1):301-11. doi: 10.1007/s11481-012-9427-3. Epub 2012 Dec 14.
Pubmed: (View Article at PubMed) PMID:23238794
DOI: Full-text: DOI:10.1007/s11481-012-9427-3

Astrocytes, the most numerous glial cell in the brain, have multiple functions and are key to maintenance of homeostasis in the central nervous system. Microglia are the resident immunocompetent cells in the brain and share several functions with macrophages, including their phagocytic ability. Indeed microglia are the resident phagocytes in the brain and express numerous cell surface proteins which act to enable receptor-mediated phagocytosis. However recent evidence suggests that astrocytes express some genes which permit phagocytosis of phosphatidylserine-decorated cells and this probably explains sporadic reports in the literature which suggest that astrocytes become phagocytic following brain trauma. Here we examined the potential of astrocytes to phagocytose fluorescently-labelled latex beads and amyloid-beta (Abeta) and report that they competently engulf both in a manner that relies on actin polymerization since it was inhibited by cytochalasin D. The data indicate that incubation of cultured astrocytes or microglia with Abeta increased phagocytosis and markers of activation of both cell types. Abeta was found to markedly increase expression of the putative Abeta-binding receptors CD36 and CD47 in astrocytes, while it decreased expression of the receptor for advanced glycation endproducts (RAGE). It is demonstrated that blocking these receptors using a neutralizing antibody attenuated Abeta-induced phagocytosis of latex beads by astrocytes. Interestingly blocking these receptors also decreased uptake of beads even in the absence of Abeta. Here we demonstrate that astrocytes are competent phagocytes and are capable of engulfing Abeta.


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CRRD Object Information
CRRD ID: 8696010
Created: 2014-08-08
Species: All species
Last Modified: 2014-08-08
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.