ArticleJournal of cell science2014
P2Y₆ receptor inhibition perturbs CCL2-evoked signalling in human monocytic and peripheral blood mononuclear cells.
Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- The role of natural polyphenols in purinergic signaling: from molecular mechanisms to physiological implications.Purinergic signalling · 2026Review
- Dual Roles of CD147 in Regulating THP-1 Monocyte Migration and MCP-1-Induced Inflammatory Responses.International journal of molecular sciences · 2025Article
- Systematic P2Y receptor survey identifies P2Y11 as modulator of immune responses and virus replication in macrophages.The EMBO journal · 2023Article
- Pannexin1: insight into inflammatory conditions and its potential involvement in multiple organ dysfunction syndrome.Frontiers in immunology · 2023Review
- Mechanisms of sympathoexcitationFrontiers in pharmacology · 2022Article
- Review
- Pannexin Channel Regulation of Cell Migration: Focus on Immune Cells.Frontiers in immunology · 2021Review
- Phosphoinositide 3-kinase γ deficiency attenuates kidney injury and fibrosis in angiotensin II-induced hypertension.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020Article
- ADP exerts P2YJournal of cell communication and signaling · 2020Article
- On the mechanism of anti-CD39 immune checkpoint therapy.Journal for immunotherapy of cancer · 2020Review
- Purinergic Signaling in Controlling Macrophage and T Cell Functions During Atherosclerosis Development.Frontiers in immunology · 2020Review
- Inhibitors of DAG metabolism suppress CCR2 signalling in human monocytes.British journal of pharmacology · 2019Article
- P2YBritish journal of pharmacology · 2018Article
- ATP Evokes CaJournal of immunology (Baltimore, Md. : 1950) · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The chemokine CCL2 serves to target circulating monocytes and other leukocytes to tissue during innate immune responses, and modulates the progression of chronic inflammatory disease through activation of the receptor CCR2. Here, we show that co-activation of the P2Y₆ purinergic receptor (encoded by P2RY₆) occurs when THP-1 cells and human peripheral blood mononuclear cells sense CCL2 through CCR2. Furthermore, P2Y₆ receptor activation accounts for ∼80% of the intracellular Ca²⁺ signal evoked by CCL2. Scavenging extracellular nucleotides with apyrase caused a fourfold reduction in THP-1 sensitivity to CCL2, whereas inhibition of CD39-like ectonucleotidases potentiated CCL2-evoked Ca²⁺ responses. Pharmacological inhibition of P2Y₆ impaired CCL2-evoked Ca²⁺ signalling and chemotaxis in peripheral blood mononuclear cells and THP-1 cells. Furthermore, stable P2Y₆ receptor knockdown (of twofold) in THP-1 cells impaired CCL2-evoked Ca²⁺ signalling, chemotaxis and adhesion to TNFα-treated HUVECs. We demonstrate that THP-1 cells rapidly secrete ATP during signalling downstream of the CCL2-CCR2 axis and suggest this might act as a mechanism for P2Y₆ receptor co-activation following CCL2 activation of the CCR2 receptor. The discovery that P2Y₆ receptor mediates leukocyte responsiveness to CCL2 represents a new mechanism by which to modulate CCL2 signals.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.