Activation of Microglia by Amyloid β Requires P2X7 Receptor Expression | Zendy

Juana María Sanz | Zendy; Paola Chiozzi | Zendy; Davide Ferrari | Zendy; Marilena Colaianna | Zendy; Marco Idzko | Zendy; Simonetta Falzoni | Zendy; R. Fellin | Zendy; Luigia Trabace | Zendy; Francesco Di Virgilio | Zendy

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Activation of Microglia by Amyloid β Requires P2X7 Receptor Expression

Author(s) -

Juana María Sanz,

Paola Chiozzi,

Davide Ferrari,

Marilena Colaianna,

Marco Idzko,

Simonetta Falzoni,

R. Fellin,

Luigia Trabace,

Francesco Di Virgilio

Publication year - 2009

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.0803612

Subject(s) - purinergic receptor , microglia , microbiology and biotechnology , extracellular , autocrine signalling , receptor , proinflammatory cytokine , intracellular , biology , amyloid (mycology) , paracrine signalling , p2y receptor , neurodegeneration , inflammation , immunology , medicine , biochemistry , disease , botany

Extracellular ATP is a mediator of intercellular communication and a danger signal. Release of this and other nucleotides modulates microglia responses via P2Y and P2X receptors, among which the P2X(7) subtype stands out for its proinflammatory activity and for up-regulation in a transgenic model of Alzheimer disease and in brains from Alzheimer disease patients. Here we show that amyloid beta (Abeta) triggered increases in intracellular Ca(2+) ([Ca(2+)](i)), ATP release, IL-1beta secretion, and plasma membrane permeabilization in microglia from wild-type but not from P2X(7)-deleted mice. Likewise, intra-hippocampal injection of Abeta caused a large accumulation of IL-1beta in wild-type but not in P2X(7)(-/-) mice. These observations suggest that Abeta activates a purinergic autocrine/paracrine stimulatory loop of which the P2X(7) receptor is an obligate component. Identification of the P2X(7) receptor as a non-dispensable factor of Abeta-mediated microglia stimulation may open new avenues for the treatment of Alzheimer disease.

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