ArticleFrontiers in immunology2018
The G2A Receptor Controls Polarization of Macrophage by Determining Their Localization Within the Inflamed Tissue.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- GPR132 antagonists alleviate atherosclerosis by suppressing M1 polarization and subsequent VSMCs proliferation and migration as revealed by transcriptomic profiling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Parabacteroides goldsteinii and its metabolite 7-KLCA attenuate endometriosis via TGR5 to reprogram macrophages by modulating the PPARγ/GPR132 axis.NPJ biofilms and microbiomes · 2026Article
- pH sensing and inflammation: linking acidic microenvironments to immune reprogramming.Frontiers in immunology · 2026Review
- Update on the impact of lipid and glucose control on diabetic wound healing.Metabolism open · 2025Review
- Efferocytosis: the art of cellular clearance and novel perspectives in disease therapy.Molecular cancer · 2025Review
- Prognostic significance of GPR132 in papillary thyroid carcinoma: insights from integrated machine learning and its role in regulating TPC-1 cell growth.Discover oncology · 2025Article
- Lactate and lactylation in tumor immunity.Frontiers of medicine · 2025Review
- Proton-Sensing G Protein-Coupled Receptors and Their Potential Role in Exercise Regulation of Arterial Function.Biomolecules · 2025Review
- GPR132 regulates the function of NK cells through the Gαs/CSK/ZAP70/NF-κB signaling pathway as a potential immune checkpoint.Science advances · 2025Article
- The inflammatory architecture reflects the effects of pharmacological and genetic interventions on resolution of TLR2-mediated inflammation.Frontiers in immunology · 2025Article
- The function of GPCRs in different bone cells.International journal of biological sciences · 2025Review
- Targeting Lactate: An Emerging Strategy for Macrophage Regulation in Chronic Inflammation and Cancer.Biomolecules · 2024Review
- Immunomodulation of Proton-activated G Protein-coupled Receptors in Inflammation.Current medical science · 2024Review
- Mast cell-derived interleukin-4 mediates activation of dendritic cell during toll-like receptor 2-mediated inflammation.Frontiers in immunology · 2024Article
- Multi-Omics Analysis of Lung Tissue Demonstrates Changes to Lipid Metabolism during Allergic Sensitization in Mice.Metabolites · 2023Article
- Eosinophil-derived IL-4 is necessary to establish the inflammatory structure in innate inflammation.EMBO molecular medicine · 2023Article
- Loss of the mammalian G-protein coupled receptor, G2A, modulates severity of invasive pulmonary aspergillosis.Frontiers in immunology · 2023Article
- Patients with Bacterial Sepsis Are Heterogeneous with Regard to Their Systemic Lipidomic Profiles.Metabolites · 2022Article
- Quantifying the inflammatory secretome of human intermuscular adipose tissue.Physiological reports · 2022Article
- T-Cell-Specific CerS4 Depletion Prolonged Inflammation and Enhanced Tumor Burden in the AOM/DSS-Induced CAC Model.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are highly versatile cells, which acquire, depending on their microenvironment, pro- (M1-like), or antiinflammatory (M2-like) phenotypes. Here, we studied the role of the G-protein coupled receptor G2A (GPR132), in chemotactic migration and polarization of macrophages, using the zymosan-model of acute inflammation. G2A-deficient mice showed a reduced zymosan-induced thermal hyperalgesia, which was reversed after macrophage depletion. Fittingly, the number of M1-like macrophages was reduced in the inflamed tissue in G2A-deficient mice. However, G2A activation was not sufficient to promote M1-polarization in bone marrow-derived macrophages. While the number of monocyte-derived macrophages in the inflamed paw was not altered, G2A-deficient mice had less macrophages in the direct vicinity of the origin of inflammation, an area marked by the presence of zymosan, neutrophil accumulation and proinflammatory cytokines. Fittingly neutrophil efferocytosis was decreased in G2A-deficient mice and several lipids, which are released by neutrophils and promote G2A-mediated chemotaxis, were increased in the inflamed tissue. Taken together, G2A is necessary to position macrophages in the proinflammatory microenvironment surrounding the center of inflammation. In absence of G2A the macrophages are localized in an antiinflammatory microenvironment and macrophage polarization is shifted toward M2-like macrophages.
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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.