ArticleThe Journal of biological chemistry2013
Pannexin 1 channels link chemoattractant receptor signaling to local excitation and global inhibition responses at the front and back of polarized neutrophils.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 97 citations in OpenAlex.
- Mitochondria regulate neutrophil activation by generating ATP for autocrine purinergic signaling.The Journal of biological chemistry · 2014Trial
- Ultrastructural Characterization of Pannexin 1 Expression Along the Rat Nephron.International journal of molecular sciences · 2026Article
- Adenosine accumulation in the blood of newborn mice weakens antimicrobial host defenses.Journal of leukocyte biology · 2025Article
- The impact of Panx1 on inflammation, immunity, and cancer: a comprehensive review.Frontiers in medicine · 2025Review
- Dual Regulatory Roles of Pannexin 1 in the Pathogenesis and Recovery of Sepsis-Induced Acute Lung Injury.Infection and drug resistance · 2025Review
- The P2YPurinergic signalling · 2024Article
- Cardiomyocyte PANX1 Controls Glycolysis and Neutrophil Recruitment in Hypertrophy.Circulation research · 2024Article
- Adenosine Triphosphate Release From Influenza-Infected Lungs Enhances Neutrophil Activation and Promotes Disease Progression.The Journal of infectious diseases · 2024Article
- Impaired ATP hydrolysis in blood plasma contributes to age-related neutrophil dysfunction.Immunity & ageing : I & A · 2024Article
- The emerging role for neutrophil mitochondrial metabolism in lung inflammation.Immunometabolism (Cobham, Surrey) · 2024Review
- ATP breakdown in plasma of children limits the antimicrobial effectiveness of their neutrophils.Purinergic signalling · 2023Article
- Neutrophil swarming: Is a good offense the best defense?iScience · 2023Review
- Pannexin1: insight into inflammatory conditions and its potential involvement in multiple organ dysfunction syndrome.Frontiers in immunology · 2023Review
- Optimized flow cytometry assays to monitor neutrophil activation in human and mouse whole blood samples.Journal of immunological methods · 2023Article
- Neutrophil trafficking to the site of infection requires Cpt1a-dependent fatty acid β-oxidation.Communications biology · 2022Article
- Optimized HPLC method to elucidate the complex purinergic signaling dynamics that regulate ATP, ADP, AMP, and adenosine levels in human blood.Purinergic signalling · 2022Article
- The Purinergic Landscape of Non-Small Cell Lung Cancer.Cancers · 2022Review
- Released ATP Mediates Spermatozoa Chemotaxis Promoted by Uterus-Derived Factor (UDF) inInternational journal of molecular sciences · 2022Article
- Functional implications of neutrophil metabolism during ischemic tissue repair.Current opinion in pharmacology · 2022Review
- Pannexin1 channels-a potential therapeutic target in inflammation.Frontiers in cell and developmental biology · 2022Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Neutrophil chemotaxis requires excitatory signals at the front and inhibitory signals at the back of cells, which regulate cell migration in a chemotactic gradient field. We have previously shown that ATP release via pannexin 1 (PANX1) channels and autocrine stimulation of P2Y2 receptors contribute to the excitatory signals at the front. Here we show that PANX1 also contributes to the inhibitory signals at the back, namely by providing the ligand for A2A adenosine receptors. In resting neutrophils, we found that A2A receptors are uniformly distributed across the cell surface. In polarized cells, A2A receptors redistributed to the back where their stimulation triggered intracellular cAMP accumulation and protein kinase A (PKA) activation, which blocked chemoattractant receptor signaling. Inhibition of PANX1 blocked A2A receptor stimulation and cAMP accumulation in response to formyl peptide receptor stimulation. Treatments that blocked endogenous A2A receptor signaling impaired the polarization and migration of neutrophils in a chemotactic gradient field and resulted in enhanced ERK and p38 MAPK signaling in response to formyl peptide receptor stimulation. These findings suggest that chemoattractant receptors require PANX1 to trigger excitatory and inhibitory signals that synergize to fine-tune chemotactic responses at the front and back of neutrophils. PANX1 channels thus link local excitatory signals to the global inhibitory signals that orchestrate chemotaxis of neutrophils in gradient fields.
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Registered trials
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.