Evidence map›Paper›PMID 18618022›Full record

ArticleThe Journal of clinical investigation2008

Ang II-stimulated migration of vascular smooth muscle cells is dependent on LR11 in mice.

Meizi Jiang, Hideaki Bujo, Kenji Ohwaki, Hiroyuki Unoki, Hiroyuki Yamazaki, Tatsuro Kanaki, Manabu Shibasaki, Kazuhiko Azuma, Kenichi Harigaya, Wolfgang J Schneider and 1 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. LR11/SorLA and its role in cardiovascular disease.International journal of cardiology. Heart & vasculature · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Observational
  8. Soluble SORLA Enhances Neurite Outgrowth and Regeneration through Activation of the EGF Receptor/ERK Signaling Axis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  9. Article
  10. Article
  11. Soluble form of LR11 is highly increased in the vitreous fluids of patients with idiopathic epiretinal membrane.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Vitreous fluid and circulating levels of soluble lr11, a novel marker for progression of diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2013
    Article
  17. Article
  18. Review
  19. Apolipoprotein E receptors in the nervous system.Current opinion in lipidology · 2009
    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

11 authors.

Meizi JiangDepartment of Genome Research and Clinical Application, Chiba University Graduate School of Medicine, Chiba, Japan.
Hideaki Bujo
Kenji Ohwaki
Hiroyuki Unoki
Hiroyuki Yamazaki
Tatsuro Kanaki
Manabu Shibasaki
Kazuhiko Azuma
Kenichi Harigaya
Wolfgang J Schneider
Yasushi Saito

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Medial-to-intimal migration of SMCs is critical to atherosclerotic plaque formation and remodeling of injured arteries. Considerable amounts of the shed soluble form of the LDL receptor relative LR11 (sLR11) produced by intimal SMCs enhance SMC migration in vitro via upregulation of urokinase-type plasminogen activator receptor (uPAR) expression. Here, we show that circulating sLR11 is a novel marker of carotid intima-media thickness (IMT) and that targeted disruption of the LR11 gene greatly reduces intimal thickening of arteries through attenuation of Ang II-induced migration of SMCs. Serum concentrations of sLR11 were positively correlated with IMT in dyslipidemic subjects, and multivariable regression analysis suggested sLR11 levels as an index of IMT, independent of classical atherosclerosis risk factors. In Lr11-/- mice, femoral artery intimal thickness after cuff placement was decreased, and Ang II-stimulated migration and attachment of SMCs from these mice were largely abolished. In isolated murine SMCs, sLR11 caused membrane ruffle formation via activation of focal adhesion kinase/ERK/Rac1 accompanied by complex formation between uPAR and integrin alphavbeta3, a process accelerated by Ang II. Overproduction of sLR11 decreased the sensitivity of Ang II-induced activation pathways to inhibition by an Ang II type 1 receptor blocker in mice. Thus, we demonstrate a requirement for sLR11 in Ang II-induced SMC migration and propose what we believe is a novel role for sLR11 as a biomarker of carotid IMT.

Indexed as

Angiotensin IIAnimalsBiomarkersCell MovementCells, CulturedCulture Media, ConditionedDose-Response Relationship, DrugMembrane Transport ProteinsMiceMice, KnockoutModels, BiologicalMuscle, Smooth, VascularReceptors, LDLSolubilityTime FactorsAngiotensin IIBiomarkersCulture Media, ConditionedMembrane Transport ProteinsReceptors, LDLSorl1 protein, mouse

Identifiers

PMID18618022
PMCPMC2447934

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.