Evidence map›Paper›PMID 31437425›Full record

ArticleThe American journal of pathology2019

Proresolving Mediators LXB4 and RvE1 Regulate Inflammation in Stromal Cells from Patients with Shoulder Tendon Tears.

Stephanie G Dakin, Romain A Colas, Kim Wheway, Bridget Watkins, Louise Appleton, Jonathan Rees, Stephen Gwilym, Christopher Little, Jesmond Dalli, Andrew J Carr

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Review
  3. A signaling network map of Lipoxin (LXA4): an anti-inflammatory molecule.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Inflammation, lipids, and pain in vulvar disease.Pharmacology & therapeutics · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Untargeted metabolomics analysis identifies creatine, myo-inositol, and lipid pathway modulation in a murine model of tendinopathy.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022
    Article
  14. Article
  15. Review
  16. Loss of 15-lipoxygenase disrupts TCell death and differentiation · 2021
    Article
  17. Local shifts in inflammatory and resolving lipid mediators in response to tendon overuse.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Stephanie G DakinNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Oxford, United Kingdom. Electronic address: stephanie.dakin@ndorms.ox.ac.uk.
Romain A ColasLipid Mediator Unit, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Kim WhewayNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Oxford, United Kingdom.
Bridget WatkinsNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Oxford, United Kingdom.
Louise AppletonNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Oxford, United Kingdom.
Jonathan ReesNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Oxford, United Kingdom.
Stephen GwilymNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Oxford, United Kingdom.
Christopher LittleNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Oxford, United Kingdom.
Jesmond DalliLipid Mediator Unit, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom; Centre for inflammation and Therapeutic Innovation, Queen Mary University of London, London, United Kingdom.
Andrew J CarrNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Oxford, United Kingdom.
University of Oxford · GBNuffield Orthopaedic Centre · GBWilliam Harvey Research Institute · GB

Funding

Department of Health II-LB-0715-20001Medical Research Council MC_PC_14103Medical Research Council MR/J006815/1Medical Research Council MR/R015651/1Wellcome Trust 107613/Z/15/Z
6 · The paper itself

Abstract

Tendon stromal cells isolated from patients with chronic shoulder rotator cuff tendon tears have dysregulated resolution responses. Current therapies do not address the biological processes concerned with persistent tendon inflammation; therefore, new therapeutic approaches that target tendon stromal cells are required. We examined whether two specialized proresolving mediators (SPMs), lipoxin B4 (LXB4) and resolvin E1 (RvE1), modulate the bioactive lipid mediator profiles of IL-1β-stimulated tendon cells derived from patients with shoulder tendon tears and healthy volunteers. We also examined whether LXB4 or RvE1 treatments moderated the proinflammatory phenotype of tendon tear stromal cells. Incubation of IL-1β-treated patient-derived tendon cells in LXB4 or RvE1 up-regulated concentrations of SPMs. RvE1 treatment of diseased tendon stromal cells increased 15-epi-LXB4 and regulated postaglandin F2α. LXB4 or RvE1 also induced expression of the SPM biosynthetic enzymes 12-lipoxygenase and 15-lipoxygenase. RvE1 treatment up-regulated the proresolving receptor human resolvin E1 compared with vehicle-treated cells. Incubation in LXB4 or RvE1 moderated the proinflammatory phenotype of patient-derived tendon tear cells, regulating markers of tendon inflammation, including podoplanin, CD90, phosphorylated signal transducer and activator of transcription 1, and IL-6. LXB4 and RvE1 counterregulate inflammatory processes in tendon stromal cells, supporting the role of these molecules as potential therapeutics to resolve tendon inflammation.

Indexed as

AgedAnti-Inflammatory AgentsCells, CulturedEicosapentaenoic AcidFemaleHumansInflammationInflammation MediatorsLacerationsLipoxinsMaleMiddle AgedShoulderShoulder InjuriesShoulder JointStromal Cells5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acidAnti-Inflammatory AgentsEicosapentaenoic AcidInflammation Mediatorslipoxin B4Lipoxins

Identifiers

PMID31437425
PMCPMC6876268
OpenAlexW2965983954

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.