Evidence map›Paper›PMID 25535917›Full record

ArticleDevelopmental cell2014

Repression of Sox9 by Jag1 is continuously required to suppress the default chondrogenic fate of vascular smooth muscle cells.

Anaïs Briot, Artur Jaroszewicz, Carmen M Warren, Jing Lu, Marlin Touma, Carsten Rudat, Jennifer J Hofmann, Rannar Airik, Gerry Weinmaster, Karen Lyons and 4 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Developmental cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  15. Article
  16. Mechanisms of fibrous cap formation in atherosclerosis.Frontiers in cardiovascular medicine · 2023
    Review
  17. Article
  18. Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022
    Review
  19. Article
  20. MicroRNA-34a: the bad guy in age-related vascular diseases.Cellular and molecular life sciences : CMLS · 2021
    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

14 authors at 2 institutions in 2 countries.

Anaïs BriotDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Artur JaroszewiczDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Carmen M WarrenDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Jing LuDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Marlin ToumaDivision of Anesthesiology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Carsten RudatInstitut fur Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany.
Jennifer J HofmannMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Rannar AirikInstitut fur Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany.
Gerry WeinmasterMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Karen LyonsDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Yibin WangDivision of Anesthesiology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Andreas KispertInstitut fur Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany.
Matteo PellegriniDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
M Luisa Iruela-ArispeDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: arispe@mcdb.ucla.edu.
University of California, Los Angeles · USMedizinische Hochschule Hannover · DE

Funding

Training Grant in Genomic Analysis and InterpretationT32HG002536 · NHGRI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Valerie A Arboleda, Harold Pimentel · 2002 to 2026
$8.6M
Vascular Biology Training GrantT32HL069766 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2002 to 2022
$7.4M
Induction of Vascular MorphogenesisR01HL114086 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOUCHARD, LOUIS, IRUELA-ARISPE, M. LUISA · 2013 to 2016
$2.1M
Notch Signaling in Vascular Development and HomeostasisR01HL085618 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI IRUELA-ARISPE, M. LUISA · 2007 to 2011
$1.9M
NHGRI NIH HHS T32 HG002536NHLBI NIH HHS R01 HL085618NHLBI NIH HHS R01 HL114086NHLBI NIH HHS T32 HL069766
6 · The paper itself

Abstract

Acquisition and maintenance of vascular smooth muscle fate are essential for the morphogenesis and function of the circulatory system. Loss of contractile properties or changes in the identity of vascular smooth muscle cells (vSMCs) can result in structural alterations associated with aneurysms and vascular wall calcification. Here we report that maturation of sclerotome-derived vSMCs depends on a transcriptional switch between mouse embryonic days 13 and 14.5. At this time, Notch/Jag1-mediated repression of sclerotome transcription factors Pax1, Scx, and Sox9 is necessary to fully enable vSMC maturation. Specifically, Notch signaling in vSMCs antagonizes sclerotome and cartilage transcription factors and promotes upregulation of contractile genes. In the absence of the Notch ligand Jag1, vSMCs acquire a chondrocytic transcriptional repertoire that can lead to ossification. Importantly, our findings suggest that sustained Notch signaling is essential throughout vSMC life to maintain contractile function, prevent vSMC reprogramming, and promote vascular wall integrity.

Indexed as

Gene Expression Regulation, DevelopmentalActive Transport, Cell NucleusAnimalsCalcium-Binding ProteinsCartilageCell LineageChondrocytesChondrogenesisFemaleIntercellular Signaling Peptides and ProteinsJagged-1 ProteinLigandsMaleMembrane ProteinsMiceMuscle ContractionCalcium-Binding ProteinsIntercellular Signaling Peptides and ProteinsJag1 protein, mouseJagged-1 ProteinLigandsMembrane ProteinsReceptors, NotchSerrate-Jagged ProteinsSox9 protein, mouseSOX9 Transcription FactorTranscription Factors

Identifiers

PMID25535917
PMCPMC4311887
OpenAlexW1988850210

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.