Evidence map›Paper›PMID 22411986›Full record

ArticleThe Journal of biological chemistry2012

Yap1 protein regulates vascular smooth muscle cell phenotypic switch by interaction with myocardin.

Changqing Xie, Yanhong Guo, Tianqing Zhu, Jifeng Zhang, Peter X Ma, Y Eugene Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

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24 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

6 authors at 2 institutions in 2 countries.

Changqing XieCardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109, USA.
Yanhong Guo
Tianqing Zhu
Jifeng Zhang
Peter X Ma
Y Eugene Chen
University of Michigan–Ann Arbor · USCardiovascular Research Center · BR

Funding

The Role of PPAR-gamma in Vascular Lesion FormationR01HL068878 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2002 to 2019
$7.6M
Nitro-Fatty Acids and Nrf2 in Vascular RemodelingR01HL105114 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2010 to 2014
$2.6M
Nitroalkenes and Blood Pressure RegulationR01HL089544 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2008 to 2012
$2.0M
NHLBI NIH HHS HL068878NHLBI NIH HHS HL105114NHLBI NIH HHS HL89544NHLBI NIH HHS R01 HL068878NHLBI NIH HHS R01 HL089544NHLBI NIH HHS R01 HL105114
6 · The paper itself

Abstract

The Hippo-Yap (Yes-associated protein) signaling pathway has emerged as one of the critical pathways regulating cell proliferation, differentiation, and apoptosis in response to environmental and developmental cues. However, Yap1 roles in vascular smooth muscle cell (VSMC) biology have not been investigated. VSMCs undergo phenotypic switch, a process characterized by decreased gene expression of VSMC contractile markers and increased proliferation, migration, and matrix synthesis. The goals of the present studies were to investigate the relationship between Yap1 and VSMC phenotypic switch and to determine the molecular mechanisms by which Yap1 affects this essential process in VSMC biology. Results demonstrated that the expression of Yap1 was rapidly up-regulated by stimulation with PDGF-BB (a known inducer of phenotypic switch in VSMCs) and in the injured vessel wall. Knockdown of Yap1 impaired VSMC proliferation in vitro and enhanced the expression of VSMC contractile genes as well by increasing serum response factor binding to CArG-containing regions of VSMC-specific contractile genes within intact chromatin. Conversely, the interaction between serum response factor and its co-activator myocardin was reduced by overexpression of Yap1 in a dose-dependent manner. Taken together, these results indicate that down-regulation of Yap1 promotes VSMC contractile phenotype by both up-regulating myocardin expression and promoting the association of the serum response factor-myocardin complex with VSMC contractile gene promoters and suggest that the Yap1 signaling pathway is a central regulator of phenotypic switch of VSMCs.

Indexed as

AnimalsApoptosis Regulatory ProteinsBecaplerminCell MovementCell ProliferationGene Expression RegulationGene Knockdown TechniquesHEK293 CellsHumansMuscle, Smooth, VascularMyocardinMyocytes, Smooth MuscleNuclear ProteinsProto-Oncogene Proteins c-sisRatsTrans-ActivatorsApoptosis Regulatory ProteinsBecaplerminMyocardinNuclear ProteinsProto-Oncogene Proteins c-sisTrans-ActivatorsYap1 protein, ratYAP-Signaling Proteins

Identifiers

PMID22411986
PMCPMC3340286
OpenAlexW2132089035

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.