Evidence map›Paper›PMID 18662895›Full record

ArticleClinical immunology (Orlando, Fla.)2008

Granulocyte chemotaxis and disease expression are differentially regulated by GRK subtype in an acute inflammatory arthritis model (K/BxN).

Teresa K Tarrant, Rishi R Rampersad, Denise Esserman, Lisa R Rothlein, Peng Liu, Richard T Premont, Robert J Lefkowitz, David M Lee, Dhavalkumar D Patel

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The GRKs Reactome: Role in Cell Biology and Pathology.International journal of molecular sciences · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Proinflammatory Cytokines Mediate GPCR Dysfunction.Journal of cardiovascular pharmacology · 2017
    Review
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  11. Article
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  14. Review
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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

9 authors at 5 institutions in 2 countries.

Teresa K TarrantThurston Arthritis Research Center, Department of Medicine, Division of Rheumatology, Allergy and Immunology, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA. tarra002@med.unc.edu
Rishi R Rampersad
Denise Esserman
Lisa R Rothlein
Peng Liu
Richard T Premont
Robert J Lefkowitz
David M Lee
Dhavalkumar D Patel
University of North Carolina at Chapel Hill · USBrigham and Women's Hospital · USDuke University · USHoward Hughes Medical Institute · USUniversity of North Carolina Health Care · US

Funding

Post-transcriptional regulation of inflammatory arthritisP01AI065858 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BENOIST, CHRISTOPHE O. · 2006 to 2010
$11.1M
UNC BIRCWH CAREER DEVELOPMENT PROGRAMK12HD001441 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BOGGESS, KIM A · 2000 to 2019
$9.3M
G Protein Coupled Receptor Regulatory Mechanisms in ArthritisK08AI070684 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TARRANT, TERESA KATHLEEN · 2006 to 2010
$527k
NIAID NIH HHS K08 AI070684NIAID NIH HHS P01 AI 065858NIAID NIH HHS P01 AI065858NICHD NIH HHS K12 HD001441NICHD NIH HHS K12 HD01441
6 · The paper itself

Abstract

objectiveChemokine receptors are G-protein coupled receptors (GPCRs) phosphorylated by G-protein receptor kinases (GRKs) after ligand-mediated activation. We hypothesized that GRK subtypes differentially regulate granulocyte chemotaxis and clinical disease expression in the K/BxN model.

methodsClinical, histologic, and cytokine responses in GRK6-/-, GRK5-/-, GRK2+/-, and wildtype mice were evaluated using K/BxN serum transfer. Granulocyte chemotaxis was analyzed by transendothelial migration assays.

resultsBoth GRK6-/- and GRK2+/- mice had increased arthritis disease severity (p<0.001); whereas GRK5-/- was not different from controls. Acute weight loss was enhanced in GRK6-/- and GRK2+/- mice (p<0.001, days 3-10). However, GRK6-/- mice uniquely had more weight loss (>10%), elevated serum IL-6, and enhanced migration toward LTB4 and C5a in vitro.

conclusionsGRK6 and -2, but not GRK5, are involved in the pathogenesis of acute arthritis in the K/BxN model. In particular, GRK6 may dampen inflammatory responses by regulating granulocyte trafficking toward chemoattractants.

Indexed as

Chemotaxis, LeukocyteAcute DiseaseAnimalsArthritisArthritis, ExperimentalComplement C5aG-Protein-Coupled Receptor Kinase 2G-Protein-Coupled Receptor KinasesGranulocytesInterleukin-6Leukotriene B4MaleMiceMice, Inbred C57BLMice, KnockoutComplement C5aG-Protein-Coupled Receptor Kinase 2G-protein-coupled receptor kinase 6G-Protein-Coupled Receptor KinasesGRK2 protein, mouseInterleukin-6Leukotriene B4

Identifiers

PMID18662895
PMCPMC2637521
OpenAlexW2040802864

What OpenQuestion holds

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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.