Evidence map›Paper›PMID 26880204›Full record

ArticleScientific reports2016

Effect of TGF-β1 on the Migration and Recruitment of Mesenchymal Stem Cells after Vascular Balloon Injury: Involvement of Matrix Metalloproteinase-14.

Wei Zhao, Chengyan Wang, Ruixue Liu, Cuilei Wei, Juncang Duan, Kejian Liu, Shugang Li, Hong Zou, Jin Zhao, Lianghai Wang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Impact of the transforming growth factor-β pathway on vascular restenosis and its mechanism.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
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  7. Article
  8. Article
  9. Article
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  12. Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Article
  15. Article
  16. Article
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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

16 authors at 1 institution in 1 country.

Wei ZhaoDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Chengyan WangDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Ruixue LiuDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Cuilei WeiDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Juncang DuanDepartment of Cardiology, the First Affiliated Hospital, Shihezi University School of Medicine, 45 North 3rd Road, Shihezi, Xinjiang 832008, China.
Kejian LiuDepartment of Cardiology, the First Affiliated Hospital, Shihezi University School of Medicine, 45 North 3rd Road, Shihezi, Xinjiang 832008, China.
Shugang LiDepartment of Public Health, Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Hong ZouDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Jin ZhaoDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Lianghai WangDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Yan QiDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Weihua LiangDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Jinfang JiangDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Wenjie ZhangDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Lijuan PangDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Feng LiDepartment of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, 59 North 2nd Road, Shihezi, Xinjiang 832002, China.
Shihezi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Restenosis or occlusion after vascular procedures is ascribed to intimal hyperplasia. Transforming growth factor (TGF)-β1 is involved in recruitment of mesenchymal stem cells (MSCs) following arterial injury, and its release from latent TGF-binding protein by matrix metalloproteinase (MMP)-14-induced proteolysis contributes to neointima formation. However, the relationship between MMP-14 and TGF-β1 activation in restenosis is unknown. This study investigated the relationship using a rat model of balloon-induced injury. Rats were assigned to vehicle-, SB431542 (SB)-, or recombinant human (rh)TGF-β1-treated groups and examined at various time points after balloon-induced injury for expression of TGF-β1/Smad signalling pathway components, MMP-14 and MSCs markers including Nestin, CD29, and Sca1(+)CD29(+)CD11b/c(-)CD45(-). Intimal hyperplasia was reduced in SB- and rhTGF-β1-treated rats. The expression of TGF-β1, TGF-β1RI, and Smad2/3 was decreased, but the levels of phosphorylated Smad2/3 were higher in SB-treated rats than vehicle-treated after 7 days to 14 days. rhTGF-β1 administration decreased the expression of TGF-β1/Smad pathway proteins, except for TGF-β1RI. Nestin and CD29 expression and the number of Sca1(+)CD29(+)CD11b(-)CD45(-) cells were reduced, whereas MMP-14 expression was increased after SB431542 and rhTGF-β1 administration. These results suggest that TGF-β1/Smad signalling and MMP-14 act to recruit MSCs which differentiate to vascular smooth muscle cells and mesenchymal-like cells that participate in arterial repair/remodelling.

Indexed as

AnimalsCell MovementDisease Models, AnimalEndothelial CellsHumansImmunohistochemistryMatrix Metalloproteinase 14Mesenchymal Stem CellsMyocytes, Smooth MuscleNeointimaPhenotypeRatsSignal TransductionSmad ProteinsTransforming Growth Factor beta1Vascular RemodelingMatrix Metalloproteinase 14Smad ProteinsTransforming Growth Factor beta1

Identifiers

PMID26880204
PMCPMC4754777
OpenAlexW2413268137

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.