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Related Experiment Video

Updated: Apr 15, 2026

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Published on: April 13, 2017

P2Y12 expression and function in alternatively activated human microglia.

Craig S Moore¹, Ariel R Ase¹, Angham Kinsara¹

¹Division of BioMedical Sciences (C.S.M.), Neuroscience, Memorial University of Newfoundland and Labrador, St. John's, Newfoundland, Canada; Neuroimmunology Unit (C.S.M., A.A., A.K., V.T.S.R., M.M.-R., S.Y.L., P.S., A.B.-O., J.P.A.), Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec, Canada; Center for Neurologic Diseases (O.B.), Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; and Department of Pathology and Molecular Medicine (S.K.L.), Queens University, Kingston, Ontario, Canada.

Neurology(R) Neuroimmunology & Neuroinflammation

|March 31, 2015

Summary

This summary is machine-generated.

P2Y12 expression is elevated in alternatively activated (M2) human microglia, influencing their calcium responses and migration. Blocking P2Y12 offers a targeted approach for neuroinflammation treatment.

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Obtaining Human Microglia from Adult Human Brain Tissue

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Area of Science:

Neuroscience
Immunology
Cell Biology

Background:

Microglia play crucial roles in brain immunity and neuroinflammation.
P2Y12 receptor is expressed on myeloid cells, but its specific role in human microglia subtypes is not fully understood.

Purpose of the Study:

To investigate the functional significance of P2Y12 receptor expression in human microglia activation.
To determine how P2Y12 influences the properties of M1 and M2 microglia in the inflamed brain.

Main Methods:

In vitro and in situ experiments were conducted on human microglia.
P2Y12 expression and function were assessed in resting, M1, and M2 microglia.
Functional assays included calcium responses, migration, and inflammatory marker analysis.

Main Results:

P2Y12 expression is significantly increased in alternatively activated (M2) human microglia compared to resting and M1 states.
M2 microglia exhibit enhanced ADP-mediated calcium responses via P2Y12, which are blocked by antagonism.
P2Y12 antagonism reduced migration and inflammatory responses in human microglia exposed to CNS injury-related nucleotides.
P2Y12 was selectively expressed on human microglia and elevated in neuropathologic conditions associated with Th2 responses.

Conclusions:

P2Y12 is selectively upregulated on M2 microglia and contributes to their functional properties.
Targeting P2Y12 offers a potential strategy for modulating M2 microglia in neuroinflammatory diseases.
These findings provide insights into the specific roles of M2 microglia in neuroinflammation and suggest a mechanism for selective myeloid cell targeting in the CNS.