Evidence map›Paper›PMID 39920161›Full record

ArticleNature communications2025

Orphan G protein-coupled receptor GPRC5B controls macrophage function by facilitating prostaglandin E receptor 2 signaling.

Jeonghyeon Kwon, Haruya Kawase, Kenny Mattonet, Stefan Guenther, Lisa Hahnefeld, Jamal Shamsara, Jan Heering, Michael Kurz, Sina Kirchhofer, Cornelius Krasel and 10 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. The Polyphenol-EnrichedFoods (Basel, Switzerland) · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Distinct cAMP Regulation in Scleroderma Lung and Skin Myofibroblasts Governs Their Dedifferentiation via p38α Inhibition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors.

Jeonghyeon KwonDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID http://orcid.org/0009-0000-5818-0110
Haruya KawaseDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID http://orcid.org/0000-0002-8927-0896
Kenny MattonetImaging Platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID http://orcid.org/0000-0002-9705-8086
Stefan GuentherDeep sequencing platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID http://orcid.org/0000-0002-5594-4549
Lisa HahnefeldFraunhofer Institute for Translational Medicine and Pharmacology ITMP, Frankfurt am Main, Germany.
Jamal ShamsaraDepartment of Pharmaceutical Chemistry, University of Marburg, Marburg, Germany.
Jan HeeringFraunhofer Institute for Translational Medicine and Pharmacology ITMP, Frankfurt am Main, Germany.ORCID http://orcid.org/0000-0002-4922-1993
Michael KurzDepartment of Pharmacology and Clinical Pharmacy, University of Marburg, Marburg, Germany.ORCID http://orcid.org/0000-0003-0326-2404
Sina KirchhoferDepartment of Pharmacology and Clinical Pharmacy, University of Marburg, Marburg, Germany.ORCID http://orcid.org/0000-0001-6285-9054
Cornelius KraselDepartment of Pharmacology and Clinical Pharmacy, University of Marburg, Marburg, Germany.ORCID http://orcid.org/0000-0001-8309-8696
Michaela UlrichDepartment of Pharmacology and Clinical Pharmacy, University of Marburg, Marburg, Germany.ORCID http://orcid.org/0009-0007-1190-4215
Margherita PersechinoDepartment of Pharmaceutical Chemistry, University of Marburg, Marburg, Germany.
Sripriya MurthyDepartment of Dermatology, Allergy, and Venereology, University of Lübeck, Lübeck, Germany.
Cesare OrlandiDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, USA.ORCID http://orcid.org/0000-0002-4992-9350
Christian D SadikDepartment of Dermatology, Allergy, and Venereology, University of Lübeck, Lübeck, Germany.ORCID http://orcid.org/0000-0001-6701-048X
Gerd GeisslingerFraunhofer Institute for Translational Medicine and Pharmacology ITMP, Frankfurt am Main, Germany.
Moritz BünemannDepartment of Pharmacology and Clinical Pharmacy, University of Marburg, Marburg, Germany.ORCID http://orcid.org/0000-0002-2259-4378
Peter KolbDepartment of Pharmaceutical Chemistry, University of Marburg, Marburg, Germany.ORCID http://orcid.org/0000-0003-4089-614X
Stefan OffermannsDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID http://orcid.org/0000-0001-8676-6805
Nina WettschureckDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany. Nina.Wettschureck@mpi-bn.mpg.de.ORCID http://orcid.org/0000-0001-6858-1460

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 204083920-SFB 1039Deutsche Forschungsgemeinschaft (German Research Foundation) 454193335-SFB 1526Deutsche Forschungsgemeinschaft (German Research Foundation) 456687919-SFB 1531
6 · The paper itself

Abstract

Macrophages express numerous G protein-coupled receptors (GPCRs) that regulate adhesion, migration, and activation, but the function of orphan receptor GPRC5B in macrophages is unknown. Both resident peritoneal and bone marrow-derived macrophages from myeloid-specific GPRC5B-deficient mice show increased migration and phagocytosis, resulting in improved bacterial clearance in a peritonitis model. In other models such as myocardial infarction, increased myeloid cell recruitment has adverse effects. Mechanistically, we found that GPRC5B physically interacts with GPCRs of the prostanoid receptor family, resulting in enhanced signaling through the prostaglandin E receptor 2 (EP2). In GPRC5B-deficient macrophages, EP2-mediated anti-inflammatory effects are diminished, resulting in hyperactivity. Using in silico modelling and docking, we identify residues potentially mediating GPRC5B/EP2 dimerization and show that their mutation results in loss of GPRC5B-mediated facilitation of EP2 signaling. Finally, we demonstrate that decoy peptides mimicking the interacting sequence are able to reduce GPRC5B-mediated facilitation of EP2-induced cAMP signaling in macrophages.

Indexed as

MacrophagesReceptors, G-Protein-CoupledReceptors, Prostaglandin E, EP2 SubtypeAnimalsCell MovementCyclic AMPHEK293 CellsHumansMaleMiceMice, Inbred C57BLMice, KnockoutMolecular Docking SimulationPeritonitisPhagocytosisSignal TransductionCyclic AMPPtger2 protein, mouseReceptors, G-Protein-CoupledReceptors, Prostaglandin E, EP2 Subtype

Identifiers

PMID39920161
PMCPMC11805951

What OpenQuestion holds

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Registered trials

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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.