Evidence map›Paper›PMID 30778537›Full record

ArticleCardiovascular research2020

Macrophage-derived MMP-8 determines smooth muscle cell differentiation from adventitia stem/progenitor cells and promotes neointima hyperplasia.

Feng Yang, Qishan Chen, Mei Yang, Eithne Margaret Maguire, Xiaotian Yu, Shiping He, Rui Xiao, Claire S Wang, Weiwei An, Wei Wu and 3 more

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

Article in Cardiovascular research, 2020. 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
5.4field-weighted citation impact, top 4% 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, 54 citations in OpenAlex.

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  7. Causal Role for Neutrophil Elastase in Thoracic Aortic Dissection in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023
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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

13 authors at 4 institutions in 2 countries.

Feng YangDepartment of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310003, Zhejiang, China.
Qishan ChenDepartment of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310003, Zhejiang, China.
Mei YangDepartment of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310003, Zhejiang, China.
Eithne Margaret MaguireWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Xiaotian YuWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Shiping HeWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Rui XiaoWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Claire S WangGonville & Caius College, University of Cambridge, Trinity Street, Cambridge, CB2 1TA, UK.
Weiwei AnWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Wei WuWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Yijiang ZhouDepartment of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310003, Zhejiang, China.
Qingzhong XiaoDepartment of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310003, Zhejiang, China.
Li ZhangDepartment of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310003, Zhejiang, China.
William Harvey Research Institute · GBZhejiang University · CNQueen Mary University of London · GBUniversity of Cambridge · GB

Funding

British Heart Foundation FS/09/044/28007British Heart Foundation PG/11/40/28891British Heart Foundation PG/13/45/30326British Heart Foundation PG/15/11/31279British Heart Foundation PG/15/86/31723British Heart Foundation PG/16/1/31892
6 · The paper itself

Abstract

aimsEmerging evidence has suggested that adventitia stem/progenitor cells (AdSPCs) migrate into the intima of arteries in response to injury, where they differentiate towards smooth muscle cells (SMCs) and participate in neointimal hyperplasia. We have previously identified matrix metalloproteinase-8 (MMP8) as a key player in atherogenesis. In this study, we aimed to investigate the functional roles of macrophage-derived MMP8 in AdSPC differentiation and injury-induced arterial remodelling. METHODS AND

resultsWe first observed an important role for MMP8 in SMC differentiation from embryonic stem cells, but this effect was not seen in AdSPCs. Instead, through macrophages/AdSPCs co-culture and macrophage conditional culture medium studies, we have demonstrated that the MMP8 protein secreted from macrophages promotes SMC differentiation from AdSPCs. Mechanistically, we showed that macrophage-derived MMP8 promotes SMC differentiation from AdSPCs through modulating transforming growth factor-β activity and a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10)/Notch1 signalling. We further demonstrated that the binding site for CBF1, Suppressor of Hairless, and Lag-1 (CSL) within SMC gene promoters is responsible for Notch1 mediated SMC differentiation. Finally, we demonstrated that macrophage-derived MMP8 increased injury-induced neointimal SMC hyperplasia by activating ADAM10/Notch1 signalling.

conclusionsWe have identified macrophage-derived MMP8 as a regulator in SMC differentiation from AdSPCs and neointimal SMC hyperplasia in response to injury. Our data provide new insights into the roles of MMP8 in AdSPC differentiation and the pathogenesis of neointima formation in the context of angiographic restenosis, and therefore may aid in the development of novel therapeutic agents for the prevention of this disease.

Indexed as

Cell DifferentiationCell ProliferationNeointimaADAM10 ProteinAdventitiaAmyloid Precursor Protein SecretasesAnimalsCarotid Artery InjuriesCells, CulturedCoculture TechniquesDisease Models, AnimalImmunoglobulin J Recombination Signal Sequence-Binding ProteinMacrophagesMatrix Metalloproteinase 8Membrane ProteinsMiceADAM10 ProteinAdam10 protein, mouseAmyloid Precursor Protein SecretasesImmunoglobulin J Recombination Signal Sequence-Binding ProteinMatrix Metalloproteinase 8Membrane ProteinsMMP8 protein, mouseNotch1 protein, mouseRbpj protein, mouseReceptor, Notch1A disintegrin and metalloproteinase domain-containing protein 10Adventitia stem cellsArterial remodellingAtherosclerosisMatrix metalloproteinase-8Neointima formationNotch signallingProgenitor cellsSmooth muscle cell differentiation

Identifiers

PMID30778537
PMCPMC6918064
OpenAlexW2917027749

What OpenQuestion 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 OpenQuestion graph.