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CpG-containing oligodeoxynucleotide promotes microglial cell uptake of amyloid beta 1-42 peptide by up-regulating the expression of the G-protein-coupled receptor mFPR2

  1. Author:
    Iribarren, P.
    Chen, K. Q.
    Hu, J. Y.
    Gong, W. H.
    Cho, E. H.
    Lockett, S.
    Uranchimeg, B.
    Wang, J. M.

  2. Author Address

    NCI, Mol Immunoregulat Lab, Canc Res Ctr, Frederick, MD 21702 USA. SAIC Frederick, Basic Res Program, Frederick, MD 21702 USA. SAIC Frederick, Image Anal Lab, Frederick, MD 21702 USA. SAIC Frederick, Dev Therapeut Program, Tumor Hypoxia Program, Frederick, MD 21702 USA Wang, JM, NCI, Mol Immunoregulat Lab, Canc Res Ctr, Bldg 560,Room 31-40, Frederick, MD 21702 USA
    1. Year: 2005
    2. Date: OCT
  2. Journal: Faseb Journal
    1. 19
    2. 12
    3. Pages: Published as FJ Express article on October 11, 2005
  4. Type of Article: Article
  1. Abstract:

    Human G protein-coupled formyl peptide receptor like 1 (FPRL1) and its mouse homologue murine formyl peptide receptor 2 (mFPR2) mediate the chemotactic activity of amyloid beta 1-42 (A beta(42)), a key pathogenic peptide in Alzheimer's disease ( AD). Since mFPR2 is up-regulated in mouse microglia by lipopolysaccharide (LPS), a Toll-like receptor 4 ligand, we investigated the capacity of CpG-containing oligodeoxynucleotide (ODN), a Toll-like receptor (TLR) 9 ligand, to regulate the expression of mFPR2 in mouse microglia. CpG ODN markedly enhanced the expression and function of mFPR2 in microglial cells, which exhibited increased chemotactic responses to mFPR2 agonists, including A beta(42). The effect of CpG ODN is dependent on activation of p38 MAPK. Further studies showed that CpG ODN-treated microglia increased their capacity to endocytose A beta(42) through mFPR2, as this process was abrogated by pertussis toxin, a Gi protein inhibitor, and W peptide, another potent mFPR2 agonist. Our results suggest that TLR9 may play an important role in promoting microglial recognition of A beta(42), thus affecting the pathogenic process of AD

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External Sources

  1. View record in Web of Science®
  2. WOS: 000232991100022

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