Evidence map›Paper›PMID 26092731›Full record

ArticleThe Journal of biological chemistry2015

A Novel Role of Matrix Metalloproteinase-8 in Macrophage Differentiation and Polarization.

Guanmei Wen, Cheng Zhang, Qishan Chen, Le Anh Luong, Arif Mustafa, Shu Ye, Qingzhong Xiao

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

36 citing papers in PubMed, 61 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Guanmei WenFrom the Centre for Clinical Pharmacology and the Department of Pathophysiology, Guangzhou Medical University, 510182 Guangzhou, China, and.
Cheng ZhangFrom the Centre for Clinical Pharmacology and the Department of Thoracic Surgery and Cardio Thoracic Surgery, The First Affiliated Hospital of Chongqing Medical University, 400016 Chongqing, China.
Qishan ChenFrom the Centre for Clinical Pharmacology and.
Le Anh LuongFrom the Centre for Clinical Pharmacology and.
Arif MustafaBiological Service Unit, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Shu YeFrom the Centre for Clinical Pharmacology and sy127@le.ac.uk.
Qingzhong XiaoFrom the Centre for Clinical Pharmacology and q.xiao@qmul.ac.uk.
Queen Mary University of London · GBWilliam Harvey Research Institute · GB

Funding

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

Abstract

Matrix metalloproteinase-8 (MMP8) has been shown to influence various cellular functions. As monocytes and macrophages (Mφ) express MMP8, we investigated if MMP8 played a role in macrophage differentiation and polarization. MMP8 expression was significantly increased during monocyte differentiation into Mφ. Monocyte-derived Mφ from MMP8-deficient mice expressed higher levels of M1-Mφ markers but lower levels of M2-Mφ markers than monocyte-derived Mφ from wild-type mice. Although Mφ from either MMP8-deficient or wild-type mice were inducible by interferon-γ into M1-Mφ, only wild-type Mφ but not MMP8-deficient Mφ could be induced into M2-Mφ by interleukin-4. However, MMP8-deficient Mφ exposed to conditioned culture media of wild-type Mφ developed a M2-Mφ phenotype. Compared with conditioned culture media of wild-type Mφ, conditioned culture media of MMP8-deficient Mφ contained a lower concentration of active transforming growth factor-β (TGF-β), an M2-Mφ inducer. Moreover, evidence also showed that the degradation of the TGF-β sequester, fibromodulin, was modulated by MMP8. The data indicate a previously unknown role of MMP8 in M2-Mφ polarization by cleaving fibromodulin and therefore increasing the bioavailability of the M2-Mφ inducer TGF-β.

Indexed as

Cell DifferentiationCell PolarityAnimalsCell LineExtracellular Matrix ProteinsFibromodulinGene Expression Regulation, EnzymologicInterleukin-4MacrophagesMatrix Metalloproteinase 8Mice, Inbred C57BLMice, KnockoutProteoglycansProteolysisSignal TransductionTransforming Growth Factor beta1Extracellular Matrix ProteinsFibromodulinFmod protein, mouseInterleukin-4Matrix Metalloproteinase 8MMP8 protein, mouseProteoglycansTransforming Growth Factor beta1extracellular matrix proteininflammationmacrophagemacrophage polarizationmatrix metalloproteinase-8matrix metalloproteinase (MMP)transforming growth factor β (TGF-β)

Identifiers

PMID26092731
PMCPMC4521038
OpenAlexW1540376590

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.