Evidence map›Paper›PMID 33311559›Full record

ArticleScientific reports2020

YY1 directly interacts with myocardin to repress the triad myocardin/SRF/CArG box-mediated smooth muscle gene transcription during smooth muscle phenotypic modulation.

Jian-Pu Zheng, Xiangqin He, Fang Liu, Shuping Yin, Shichao Wu, Maozhou Yang, Jiawei Zhao, Xiaohua Dai, Hong Jiang, Luyi Yu and 9 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  10. Circulation · 2021
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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

19 authors at 5 institutions in 3 countries.

Jian-Pu ZhengDepartment of Internal Medicine, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Xiangqin HeDepartment of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA.
Fang LiuDepartment of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA.
Shuping YinDepartment of Internal Medicine, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Shichao WuDepartment of Internal Medicine, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Maozhou YangBone and Joint Center, Henry Ford Hospital, Detroit, MI, 48202, USA.
Jiawei ZhaoDepartment of Internal Medicine, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Xiaohua DaiDepartment of Internal Medicine, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Hong JiangDepartment of Internal Medicine, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Luyi YuDepartment of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA.
Qin YinDepartment of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA.
Donghong JuDepartment of Internal Medicine, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Claire LiCenter for Molecular Medicine and Genetics, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Leonard LipovichCenter for Molecular Medicine and Genetics, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Youming XieBarbara Ann Karmanos Cancer Institute, Wayne State University, Detroit, MI, 48201, USA.
Kezhong ZhangCenter for Molecular Medicine and Genetics, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA.
Hui J LiDepartment of Medicine, University of Massachusetts, Worcester, MA, 01655, USA.
Jiliang ZhouDepartment of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA. jizhou@augusta.edu.ORCID 0000-0002-2375-4636
Li LiDepartment of Internal Medicine, Wayne State University, 421 E. Canfield Ave. #2146, Detroit, MI, 48201, USA. lili@med.wayne.edu.
Wayne State University · USAugusta University · USHenry Ford Hospital · USNanchang Institute of Technology · CNUniversity of Massachusetts Chan Medical School · US

Funding

The regulatory roles of nuclear SM22 in smooth muscle phenotypic modulationR01HL142956 · NHLBI · WAYNE STATE UNIVERSITY · PI LI, LI · 2018 to 2021
$2.1M
The novel smooth muscle-specific lncRNA CARMN is a critical regulator of smooth muscle phenotypeR01HL149995 · NHLBI · AUGUSTA UNIVERSITY · PI ZHOU, JILIANG · 2020 to 2023
$2.0M
Role of Hippo-YAP Pathway in Smooth Muscle Phenotypic ModulationR01HL109605 · NHLBI · AUGUSTA UNIVERSITY · PI ZHOU, JILIANG · 2012 to 2016
$1.8M
The Role of SM22 in the Pathogenesis of Aortic AneurysmsR01HL119815 · NHLBI · WAYNE STATE UNIVERSITY · PI LI, LI · 2014 to 2017
$1.5M
GENETIC CONTROL OF SMOOTH MUSCLE GENE EXPRESSIONR01HL058916 · NHLBI · WAYNE STATE UNIVERSITY · PI LI, LI · 1998 to 2002
$850k
NHLBI NIH HHS HL109605NHLBI NIH HHS HL119815NHLBI NIH HHS HL142956NHLBI NIH HHS HL58916NHLBI NIH HHS R01 HL058916NHLBI NIH HHS R01 HL109605NHLBI NIH HHS R01 HL119815NHLBI NIH HHS R01 HL142956NHLBI NIH HHS R01 HL149995
6 · The paper itself

Abstract

Yin Yang 1 (YY1) regulates gene transcription in a variety of biological processes. In this study, we aim to determine the role of YY1 in vascular smooth muscle cell (VSMC) phenotypic modulation both in vivo and in vitro. Here we show that vascular injury in rodent carotid arteries induces YY1 expression along with reduced expression of smooth muscle differentiation markers in the carotids. Consistent with this finding, YY1 expression is induced in differentiated VSMCs in response to serum stimulation. To determine the underlying molecular mechanisms, we found that YY1 suppresses the transcription of CArG box-dependent SMC-specific genes including SM22α, SMα-actin and SMMHC. Interestingly, YY1 suppresses the transcriptional activity of the SM22α promoter by hindering the binding of serum response factor (SRF) to the proximal CArG box. YY1 also suppresses the transcription and the transactivation of myocardin (MYOCD), a master regulator for SMC-specific gene transcription by binding to SRF to form the MYOCD/SRF/CArG box triad (known as the ternary complex). Mechanistically, YY1 directly interacts with MYOCD to competitively displace MYOCD from SRF. This is the first evidence showing that YY1 inhibits SMC differentiation by directly targeting MYOCD. These findings provide new mechanistic insights into the regulatory mechanisms that govern SMC phenotypic modulation in the pathogenesis of vascular diseases.

Indexed as

Transcription, GeneticAnimalsHeterogeneous-Nuclear Ribonucleoprotein Group A-BMaleMiceMyocardinMyocytes, Smooth MuscleNuclear ProteinsRatsRats, Sprague-DawleyRepressor ProteinsSerum Response FactorTrans-ActivatorsTranscription FactorsYY1 Transcription FactorHeterogeneous-Nuclear Ribonucleoprotein Group A-BHnrnpab protein, mouseMyocardinNuclear ProteinsRepressor ProteinsSerum Response Factorserum response factor, ratSrf protein, mouseTrans-ActivatorsTranscription FactorsYy1 protein, mouseYy1 protein, ratYY1 Transcription Factor

Identifiers

PMID33311559
PMCPMC7732823
OpenAlexW3113238046

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.