Evidence map›Paper›PMID 19906641›Full record

ArticleThe Journal of biological chemistry2010

Resolvin E1 receptor activation signals phosphorylation and phagocytosis.

Taisuke Ohira, Makoto Arita, Kazuhiro Omori, Antonio Recchiuti, Thomas E Van Dyke, Charles N Serhan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed
10.0field-weighted citation impact, top 1% of its field
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

157 citing papers in PubMed, 274 citations in OpenAlex.

  1. Resolvin E2 formation and impact in inflammation resolution.Journal of immunology (Baltimore, Md. : 1950) · 2012
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  13. Linking Lipid Metabolism and Immune Function: New Insights into Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
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97 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Taisuke OhiraDepartment of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Center for Experimental Therapeutics and Reperfusion Injury, Boston, Massachusetts 02115, USA.
Makoto Arita
Kazuhiro Omori
Antonio Recchiuti
Thomas E Van Dyke
Charles N Serhan
Harvard University · USBoston University · USBrigham and Women's Hospital · US

Funding

Specialized Center for Oral Inflammation and ResolutionP50DE016191 · NIDCR · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 2004 to 2010
$13.6M
BLOOD CELL LIPOXYGENASE PRODUCTS: FORMATION AND ACTIONR01GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 1992 to 2020
$4.9M
Neutrophils and Periodontitis in DiabetesR01DE015566 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI VAN DYKE, THOMAS ELLIOTT · 2005 to 2014
$4.2M
BLOOD CELL LIPOXYGENASE PRODUCTS--FORMATION AND ACTIONR37GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 2000 to 2009
$4.0M
BLOOD CELL LIPOXYGENASE PRODUCTS--FORMATION &ACTIONR29GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 1987 to 1991
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NIDCR NIH HHS DE-015566NIDCR NIH HHS DE-016191NIDCR NIH HHS P50 DE016191NIDCR NIH HHS R01 DE015566NIGMS NIH HHS GM38765NIGMS NIH HHS R01 GM038765NIGMS NIH HHS R37 GM038765
6 · The paper itself

Abstract

Resolvins are endogenous lipid mediators that actively regulate the resolution of acute inflammation. Resolvin E1 (RvE1; (5S,12R,18R)-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid) is an endogenous anti-inflammatory and pro-resolving mediator derived from eicosapentaenoic acid that regulates leukocyte migration and enhances macrophage phagocytosis of apoptotic neutrophils to resolve inflammation. In the inflammatory milieu, RvE1 mediates counter-regulatory actions initiated via specific G protein-coupled receptors. Here, we have identified RvE1-specific signaling pathways initiated by the RvE1 receptor ChemR23. RvE1 stimulated phosphorylation of Akt that was both ligand- and receptor-dependent. RvE1 regulated Akt phosphorylation in a time (0-15 min)- and dose-dependent (0.01-100 nm) manner in human ChemR23-transfected Chinese hamster ovary cells. RvE1 stimulated phosphorylation of both Akt and a 30-kDa protein, a downstream target of Akt, identified using a phospho-Akt substrate antibody. The 30-kDa protein was identified as ribosomal protein S6, a translational regulator, and its phosphorylation was inhibited by a phosphatidylinositol 3-kinase (PI3K) inhibitor (wortmannin) and an ERK inhibitor (PD98059) but not by a p38-MAPK inhibitor (SB203580). Ribosomal protein S6 is a downstream target of the PI3K/Akt signaling pathway as well as the Raf/ERK pathway. In ChemR23-expressing differentiated HL60 cells, RvE1 also stimulated the phosphorylation of ribosomal protein S6. In addition, RvE1 enhanced phagocytosis of zymosan A by human macrophages, which are inhibited by PD98059 and rapamycin (mTOR inhibitor). These results indicate that RvE1 initiates direct activation of ChemR23 and signals receptor-dependent phosphorylation. These phosphorylation-signaling pathways identified for RvE1 receptor-ligand interactions underscore the importance of endogenous pro-resolving agonists in resolving acute inflammation.

Indexed as

AnimalsCell DifferentiationCHO CellsCricetinaeCricetulusEicosapentaenoic AcidFlavonoidsHL-60 CellsHumansInflammationLipidsMacrophagesPhagocytosisPhosphorylationReceptors, ChemokineSirolimus2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acidCMKLR1 protein, humanEicosapentaenoic AcidFlavonoidsLipidsReceptors, ChemokineSirolimusZymosan

Identifiers

PMID19906641
PMCPMC2823415
OpenAlexW1988697119

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.