Evidence map›Paper›PMID 27760754›Full record

ArticleAmerican journal of physiology. Cell physiology2016

Lysophosphatidic acid-induced vascular neointimal formation in mouse carotid arteries is mediated by the matricellular protein CCN1/Cyr61.

Feng Hao, Fuqiang Zhang, Daniel Dongwei Wu, Dong An, Jing Shi, Guohong Li, Xuemin Xu, Mei-Zhen Cui

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

Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Matricellular proteins in atherosclerosis development.Matrix biology : journal of the International Society for Matrix Biology · 2023
    Review
  7. Article
  8. Expression of Cyr61 in ApoEScientific reports · 2021
    Article
  9. Article
  10. Article
  11. 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

8 authors at 4 institutions in 2 countries.

Feng HaoDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee.
Fuqiang ZhangDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee.
Daniel Dongwei WuDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee.
Dong AnDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee.
Jing ShiDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee.
Guohong LiDepartment of Neurosurgery, Louisiana State University Health Science Center in Shreveport, Shreveport, Louisiana.
Xuemin XuDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee.
Mei-Zhen CuiDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee; cuim@utk.edu.
University of Tennessee at Knoxville · USJilin University · CNLouisiana State University Health Sciences Center Shreveport · USShanxi University · CN

Funding

Mechanisms of CD40/CD40L in vascular injury and repairR01HL087990 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI LI, GUOHONG · 2008 to 2013
$1.6M
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 HL087990NIA NIH HHS R01 AG026640NINDS NIH HHS R21 NS095256
6 · The paper itself

Abstract

Vascular smooth muscle cell (SMC) migration is an essential step involved in neointimal formation in restenosis and atherosclerosis. Lysophosphatidic acid (LPA) is a bioactive component of oxidized low-density lipoprotein and is produced by activated platelets, implying that LPA influences vascular remodeling. Our previous study revealed that matricellular protein CCN1, a prominent extracellular matrix (ECM) protein, mediates LPA-induced SMC migration in vitro. Here we examined the role of CCN1 in LPA-induced neointimal formation. By using LPA infusion of carotid artery in a mouse model, we demonstrated that LPA highly induced CCN1 expression (approximately six- to sevenfold) in neointimal lesions. Downregulation of CCN1 expression with the specific CCN1 siRNA in carotid arteries blocked LPA-induced neointimal formation, indicating that CCN1 is essential in LPA-induced neointimal formation. We then used LPA receptor knockout (LPA

Indexed as

AnimalsCarotid Artery, CommonCell MovementCells, CulturedCysteine-Rich Protein 61Down-RegulationExtracellular Matrix ProteinsFemaleLipoproteins, LDLLysophospholipidsMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaCCN1 protein, mouseCysteine-Rich Protein 61Extracellular Matrix ProteinsLipoproteins, LDLlysophosphatidic acidLysophospholipidsoxidized low density lipoproteinReceptors, Lysophosphatidic AcidRNA, Small InterferingCCN1lysophosphatidic acidsmooth muscle cellsvascular neointimal formation

Identifiers

PMID27760754
PMCPMC5206305
OpenAlexW2533159998

What Socratic 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 Socratic graph.