Evidence map›Paper›PMID 18706682›Full record

ArticleThrombosis research2009

Deficiency of LRP8 in mice is associated with altered platelet function and prolonged time for in vivo thrombosis.

Jason O Robertson, Wei Li, Roy L Silverstein, Eric J Topol, Jonathan D Smith

Abstract read
In one paragraph

Article in Thrombosis research, 2009. 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
–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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Angiotensin II Infusion Leads to Aortic Dissection in LRP8 Deficient Mice.International journal of molecular sciences · 2020
    Article
  6. Review
  7. New Insights in the Pathophysiology of Antiphospholipid Syndrome.Seminars in thrombosis and hemostasis · 2018
    Review
  8. Ferric Chloride-induced Murine Thrombosis Models.Journal of visualized experiments : JoVE · 2016
    Article
  9. High levels of LDL-C combined with low levels of HDL-C further increase platelet activation in hypercholesterolemic patients.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2015
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Lack of association of common polymorphism of LRP1 gene with myocardial infarction in a Chinese Han population.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2011
    Article
  19. Article
  20. 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

5 authors.

Jason O RobertsonDepartment of Cell Biology, Cleveland Clinic, Cleveland, OH; Cleveland Clinic Lerner College of Medicine, Cleveland Clinic, Cleveland, OH, USA.
Wei Li
Roy L Silverstein
Eric J Topol
Jonathan D Smith

Funding

The Role of Thrombospondins in AtherothrombosisP50HL077107 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI PLOW, EDWARD FRANKLIN · 2005 to 2009
$16.5M
Howard Hughes Medical InstituteNHLBI NIH HHS P50 HL077107NHLBI NIH HHS P50-HL077107
6 · The paper itself

Abstract

introductionOur group has previously reported genetic studies associating polymorphisms in the low density lipoprotein receptor related protein 8 (LRP8) gene with myocardial infarction. The aim of this study was to define the role of platelet surface LRP8 in thrombosis. MATERIALS AND

methodsFlow cytometry, aggregometry, intravital microscopy and tail bleeding assays were used to examine platelet function and hemostasis in LRP8-deficient mice and littermate controls.

resultsWe demonstrated that activation of platelets from both LRP8(+/-) and LRP8(-/-) mice was reduced in vitro in response to either ADP or thrombin. In vivo, LRP8-hemizygous and LRP8(-/-) mice demonstrated 200% and 68% increased time for carotid occlusion in response to FeCl(3) injury, respectively. Moreover, lipidated apoE3, a ligand for LRP8, inhibited platelet activation in a dose-dependent fashion. This inhibition was markedly attenuated in LRP8(-/-) but not LRP8(+/-) mice and did not result from membrane cholesterol efflux or a nitric oxide dependent pathway. Tail bleeding times were unaffected in both genotypes.

conclusionsOur results suggest that LRP8 is capable of altering thrombosis without affecting normal hemostasis through mechanisms both dependent on and independent of apoE. This suggests a means whereby clot formation could be affected in humans with LRP8 gene variants.

Indexed as

AnimalsApolipoprotein E3Blood PlateletsChloridesFerric CompoundsHumansLDL-Receptor Related ProteinsMiceMice, KnockoutNitric OxidePlatelet ActivationReceptors, LipoproteinThrombosisApolipoprotein E3Chloridesferric chlorideFerric CompoundsLDL-Receptor Related Proteinslow density lipoprotein receptor-related protein 8Nitric OxideReceptors, Lipoprotein

Identifiers

PMID18706682
PMCPMC2661626

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.