Evidence map›Paper›PMID 24386293›Full record

ArticlePloS one2013

Increase of ADAM10 level in coronary artery in-stent restenosis segments in diabetic minipigs: high ADAM10 expression promoting growth and migration in human vascular smooth muscle cells via Notch 1 and 3.

Ke Yang, Lin Lu, Yan Liu, Qi Zhang, Li Jin Pu, Lin Jie Wang, Zhen Bing Zhu, Ya Nan Wang, Hua Meng, Xiao Jie Zhang and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Contribution of ADAM17 and related ADAMs in cardiovascular diseases.Cellular and molecular life sciences : CMLS · 2021
    Review
  8. Article
  9. 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

13 authors at 1 institution in 1 country.

Ke YangInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Lin LuInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China ; Department of Cardiology, Rui Jin Hospital, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Yan LiuInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Qi ZhangInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China ; Department of Cardiology, Rui Jin Hospital, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Li Jin PuInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Lin Jie WangInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China ; Department of Cardiology, Rui Jin Hospital, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Zhen Bing ZhuInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China ; Department of Cardiology, Rui Jin Hospital, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Ya Nan WangInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Hua MengInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Xiao Jie ZhangInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Run DuDepartment of Cardiology, Rui Jin Hospital, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Qiu Jing ChenInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Wei Feng ShenInstitute of Cardiovascular Diseases, Medical School of Jiaotong University, Shanghai, People's Republic of China ; Department of Cardiology, Rui Jin Hospital, Medical School of Jiaotong University, Shanghai, People's Republic of China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study aimed to identify major proteins in the pathogenesis of coronary artery in-stent restenosis (ISR) in diabetic minipigs with sirolimus-eluting stenting, and to investigate the roles of key candidate molecules, particularly ADAM10, in human arterial smooth muscle cells (HASMCs). METHODS AND

resultsThe stents were implanted in the coronary arteries of 15 diabetic and 26 non-diabetic minipigs, and angiography was repeated at six months. The intima of one vascular segment with significant ISR and one with non-ISR in diabetic minipigs were isolated and cultured in conditioned medium (CM). The CM was analyzed by LC-MS/MS to uncover proteins whose levels were significantly increased (≥ 1.5-fold) in ISR than in non-ISR tissues. After literature searching, we focused on the identified proteins, whose biological functions were most potentially related to ISR pathophysiology. Among them, ADAM10 was significantly increased in diabetic and non-diabetic ISR tissues as compared with non-ISR controls. In cell experiments, retrovirus-mediated overexpression of ADAM10 promoted growth and migration of HASMCs. The effects of ADAM10 were more remarkable in high-glucose culture than in low-glucose culture. Using shRNA and an inhibitor of γ-secretase (GSI), we found that the influences of ADAM10 were in part mediated by Notch1 and notch 3 pathway, which up-regulated Notch downstream genes and enhanced nuclear translocation of the small intracellular component of Notch1 and Notch3.

conclusionsThis study has identified significantly increased expression of ADAM10 in the ISR versus non-ISR segment in diabetic minipigs and implicates ADAM10 in the enhanced neointimal formation observed in diabetes after vascular injury.

Indexed as

Cell MovementStentsADAM10 ProteinADAM ProteinsAmyloid Precursor Protein SecretasesAnimalsCell ProliferationCoronary RestenosisCoronary VesselsDiabetes ComplicationsGene ExpressionHumansHyperplasiaMembrane ProteinsMuscle, Smooth, VascularNeointimaADAM10 ProteinADAM10 protein, humanADAM ProteinsAmyloid Precursor Protein SecretasesMembrane ProteinsReceptor, Notch1

Identifiers

PMID24386293
PMCPMC3873985
OpenAlexW2002269578

What OpenQuestion holds

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LicenceCC BY
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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.