Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 33, Issue 21, Pages 4282-4293Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00544-13
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Funding
- Major State Basic Research Program of China [2011CB504400]
- National Natural Science Foundation of China [31190060, 81221003, 30730037, 30870834]
- PCSIRT
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Brain disturbances, like injuries or aberrant protein deposits, evoke nucleotide release or leakage from cells, leading to microglial chemotaxis and ingestion. Recent studies have identified P2Y(12) purinergic receptors as triggers for microglial chemotaxis and P2Y(6) receptors as mediators for phagocytosis. However, pinocytosis, known as the internalization of fluid-phase materials, has received much less attention. We found that ATP efficiently triggered pinocytosis in microglia. Pharmacological analysis and knockdown experiments demonstrated the involvement of P2Y(4) receptors and the phosphatidylinositol 3-kinase/Akt cascade in the nucleotide-induced pinocytosis. Further evidence indicated that soluble amyloid beta peptide 1-42 induced self-uptake in microglia through pinocytosis, a process involving activation of P2Y(4) receptors by autocrine ATP signaling. Our results demonstrate a previously unknown function of ATP as a drink me signal for microglia and P2Y(4) receptors as a potential therapeutic target for the treatment of Alzheimer's disease.
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