Evidence map›Paper›PMID 27053419›Full record

ArticleScientific reports2016

Deficiency of the TLR4 analogue RP105 aggravates vein graft disease by inducing a pro-inflammatory response.

Anouk Wezel, Margreet R de Vries, Johanna M Maassen, Peter Kip, Erna A Peters, Jacco C Karper, Johan Kuiper, Ilze Bot, Paul H A Quax

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
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  6. Review
  7. Review
  8. Article
  9. Inflammation in Vein Graft Disease.Frontiers in cardiovascular medicine · 2018
    Review
  10. Review
  11. Article
  12. Review
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 2 institutions in 1 country.

Anouk WezelDivision of Biopharmaceutics, LACDR, Leiden University, Leiden, The Netherlands.
Margreet R de VriesDepartment of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
Johanna M MaassenDivision of Biopharmaceutics, LACDR, Leiden University, Leiden, The Netherlands.
Peter KipDepartment of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
Erna A PetersDepartment of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
Jacco C KarperDepartment of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
Johan KuiperDivision of Biopharmaceutics, LACDR, Leiden University, Leiden, The Netherlands.
Ilze BotDivision of Biopharmaceutics, LACDR, Leiden University, Leiden, The Netherlands.
Paul H A QuaxDepartment of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
Leiden University Medical Center · NLLeiden University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Venous grafts are often used to bypass occlusive atherosclerotic lesions; however, poor patency leads to vein graft disease. Deficiency of TLR4, an inflammatory regulator, reduces vein graft disease. Here, we investigate the effects of the accessory molecule and TLR4 analogue RadioProtective 105 (RP105) on vein graft disease. RP105 deficiency resulted in a 90% increase in vein graft lesion area compared to controls. In a hypercholesterolemic setting (LDLr(-/-)/RP105(-/-) versus LDLr(-/-) mice), which is of importance as vein graft disease is usually characterized by excessive atherosclerosis, total lesion area was not affected. However we did observe an increased number of unstable lesions and intraplaque hemorrhage upon RP105 deficiency. In both setups, lesional macrophage content, and lesional CCL2 was increased. In vitro, RP105(-/-) smooth muscle cells and mast cells secreted higher levels of CCL2. In conclusion, aggravated vein graft disease caused by RP105 deficiency results from an increased local inflammatory response.

Indexed as

AnimalsAntigens, CDAtherosclerosisCells, CulturedChemokine CCL2Gene ExpressionImmunohistochemistryInflammation MediatorsMacrophagesMast CellsMatrix MetalloproteinasesMice, Inbred C57BLMice, KnockoutMyocytes, Smooth MuscleReceptors, LDLReverse Transcriptase Polymerase Chain ReactionAntigens, CDCcl2 protein, mouseChemokine CCL2Inflammation MediatorsLy78 protein, mouseMatrix MetalloproteinasesReceptors, LDLTissue Inhibitor of Metalloproteinases

Identifiers

PMID27053419
PMCPMC4823661
OpenAlexW2313060681

What OpenQuestion holds

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LicenceCC BY
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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.