Evidence map›Paper›PMID 28157379›Full record

ArticleCanadian journal of physiology and pharmacology2017

CRE and SRE mediate LPA-induced CCN1 transcription in mouse aortic smooth muscle cells.

Quanlin Dou, Feng Hao, Longsheng Sun, Xuemin Xu, Mei-Zhen Cui

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

Article in Canadian journal of physiology and pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 90% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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

5 authors at 2 institutions in 2 countries.

Quanlin Doua Department of Biomedical & Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA.
Feng Haoa Department of Biomedical & Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA.
Longsheng Suna Department of Biomedical & Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA.
Xuemin Xua Department of Biomedical & Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA.
Mei-Zhen Cuia Department of Biomedical & Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA.
Knoxville College · USQinghai University · CN

Funding

Novel mechanism mediating LPA-induced smooth muscle cell and vascular responsesR01HL107466 · NHLBI · UNIVERSITY OF TEXAS OF THE PERMIAN BASIN · PI CUI, MEI-ZHEN · 2011 to 2020
$3.3M
The role of the new zeta-cleavage in Abeta formationR01AG026640 · NIA · UNIVERSITY OF TENNESSEE KNOXVILLE · PI XU, XUEMIN · 2007 to 2011
$1.4M
Pathogenic ROle of the Novel Mitochondrial Apoptotic PSAP in ALSR21NS095256 · NINDS · UNIVERSITY OF TEXAS OF THE PERMIAN BASIN · PI CUI, MEI-ZHEN · 2016 to 2017
$404k
NHLBI NIH HHS R01 HL107466NIA NIH HHS R01 AG026640NINDS NIH HHS R21 NS095256
6 · The paper itself

Abstract

Lysophosphatidic acid (LPA), one component of oxidized low-density lipoprotein (ox-LDL), is a potent bioactive phospholipid. Our recent data reveal that LPA induces matricellular protein CCN1 (also known as Cyr61) expression in aortic smooth muscle cells (SMCs) and that CCN1 bridges LPA and integrin signaling pathways leading to SMC migration. Whether and how LPA regulates the transcriptional machinery of the CCN1 gene are unknown. In this study, we found that LPA markedly induces CCN1 mRNA expression in SMCs. Using deleting mutation and reporter gene strategies, we demonstrated regions from -2038 to -1787 and from -101 to +63 of the CCN1 promoter contain the essential regulatory elements. The serum response element (SRE) and cyclic AMP-response element (CRE) are located in these regions. LPA induced time-dependent phosphorylation of serum response factor (SRF) and CRE-binding protein (CREB) in mouse SMCs. Luciferase assays of a series of deleted, mutated CCN1 promoter-reporter gene constructs and dominant negative construct revealed the distal SRE and the proximal CRE in the CCN1 promoter are required for LPA-induced CCN1 gene expression. Our results imply that elevated LPA levels may trigger SMC migration and exacerbate restenosis and atherosclerotic lesions through the induced CCN1, which communicates with a set of plasma membrane proteins and intracellular kinases.

Indexed as

AnimalsAortaBinding SitesCells, CulturedCyclic AMP Response Element-Binding ProteinCysteine-Rich Protein 61Genes, ReporterLysophospholipidsMiceMuscle, Smooth, VascularMyocytes, Smooth MusclePhosphorylationProtein BindingRNA, MessengerSerum Response ElementSerum Response FactorCCN1 protein, mouseCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinCysteine-Rich Protein 61lysophosphatidic acidLysophospholipidsRNA, MessengerSerum Response Factoracide lysophosphatidiqueaortic smooth muscle cellsCCN1cellules musculaires lisses aortiquesgene regulationlysophosphatidic acidrégulation géniquetranscription

Identifiers

PMID28157379
PMCPMC5644987
OpenAlexW2563443113

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.