Evidence map›Paper›PMID 18818417›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2008

Notch3 is a major regulator of vascular tone in cerebral and tail resistance arteries.

E J Belin de Chantemèle, K Retailleau, F Pinaud, E Vessières, A Bocquet, A L Guihot, B Lemaire, V Domenga, C Baufreton, L Loufrani and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 109 citations in OpenAlex.

  1. CADASIL mutations and shRNA silencing of NOTCH3 affect actin organization in cultured vascular smooth muscle cells.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012
    Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Progress to Clarify HowBiomolecules · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 1 country.

E J Belin de ChantemèleINSERM U 771, Angers, France.
K Retailleau
F Pinaud
E Vessières
A Bocquet
A L Guihot
B Lemaire
V Domenga
C Baufreton
L Loufrani
A Joutel
D Henrion
Centre Hospitalier Universitaire d'Angers · FRInserm · FR

Funding

Notch3 signaling in small-artery-diseasesR01NS054122 · NINDS · NAT'L INST OF HLTH/MED RES INSERM-PARIS · PI JOUTEL, ANNE · 2006 to 2009
$666k
NINDS NIH HHS R01 NS 054122NINDS NIH HHS R01 NS054122
6 · The paper itself

Abstract

objectiveNotch3, a member of the evolutionary conserved Notch receptor family, is primarily expressed in vascular smooth muscle cells. Genetic studies in human and mice revealed a critical role for Notch3 in the structural integrity of distal resistance arteries by regulating arterial differentiation and postnatal maturation. METHODS AND

resultsWe investigated the role of Notch3 in vascular tone in small resistance vessels (tail and cerebral arteries) and large (carotid) arteries isolated from Notch3-deficient mice using arteriography. Passive diameter and compliance were unaltered in mutant arteries. Similarly, contractions to phenylephrine, KCl, angiotensin II, and thromboxane A2 as well as dilation to acetylcholine or sodium nitroprusside were unaffected. However, Notch3 deficiency induced a dramatic reduction in pressure-induced myogenic tone associated with a higher flow (shear stress)-mediated dilation in tail and cerebral resistance arteries only. Furthermore, RhoA activity and myosin light chain phosphorylation, measured in pressurized tail arteries, were significantly reduced in Notch3KO mice. Additionally, myogenic tone inhibition by the Rho kinase inhibitor Y27632 was attenuated in mutant tail arteries.

conclusionsNotch3 plays an important role in the control of vascular mechano-transduction, by modulating the RhoA/Rho kinase pathway, with opposite effects on myogenic tone and flow-mediated dilation in the resistance circulation.

Indexed as

AcetylcholineAmidesAnimalsArteriesCerebral ArteriesEnzyme InhibitorsMaleMiceMice, KnockoutPhenylephrinePyridinesReceptor, Notch3Receptors, NotchrhoA GTP-Binding Proteinrho-Associated Kinasesrho GTP-Binding ProteinsAcetylcholineAmidesEnzyme InhibitorsNotch3 protein, mousePhenylephrinePyridinesReceptor, Notch3Receptors, NotchrhoA GTP-Binding ProteinRhoA protein, mouserho-Associated Kinasesrho GTP-Binding ProteinsY 27632

Identifiers

PMID18818417
PMCPMC2658748
OpenAlexW2004913600

What OpenQuestion holds

Textmetadata
LicenceTDM
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.