Evidence map›Paper›PMID 32126159›Full record

ArticleJournal of cellular and molecular medicine2020

Macrophage-derived MMP-9 enhances the progression of atherosclerotic lesions and vascular calcification in transgenic rabbits.

Yajie Chen, Ahmed Bilal Waqar, Kazutoshi Nishijima, Bo Ning, Shuji Kitajima, Fumikazu Matsuhisa, Lu Chen, Enqi Liu, Tomonari Koike, Ying Yu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 75 citations in OpenAlex.

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  17. Protective effect of 6'-Sialyllactose on LPS-induced macrophage inflammationThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    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

15 authors at 9 institutions in 3 countries.

Yajie ChenDepartment of Molecular Pathology, Faculty of Medicine, Graduate School of Medical Sciences, University of Yamanashi, Yamanashi, Japan.ORCID 0000-0001-6567-0396
Ahmed Bilal WaqarDepartment of Molecular Pathology, Faculty of Medicine, Graduate School of Medical Sciences, University of Yamanashi, Yamanashi, Japan.
Kazutoshi NishijimaBioscience Education-Research Support Center, Akita University, Akita, Japan.
Bo NingDepartment of Molecular Pathology, Faculty of Medicine, Graduate School of Medical Sciences, University of Yamanashi, Yamanashi, Japan.
Shuji KitajimaAnalytical Research Center for Experimental Sciences, Saga University, Saga, Japan.
Fumikazu MatsuhisaAnalytical Research Center for Experimental Sciences, Saga University, Saga, Japan.
Lu ChenDepartment of Molecular Pathology, Faculty of Medicine, Graduate School of Medical Sciences, University of Yamanashi, Yamanashi, Japan.
Enqi LiuResearch Institute of Atherosclerotic Disease and Laboratory Animal Center, Xi'an Jiaotong University School of Medicine, Xi'an, China.
Tomonari KoikeCenter for Advanced Models for Translational Sciences and Therapeutics, University of Michigan Medical Center, Ann Arbor, MI, USA.ORCID 0000-0003-4718-8234
Ying YuCenter for Advanced Models for Translational Sciences and Therapeutics, University of Michigan Medical Center, Ann Arbor, MI, USA.ORCID 0000-0002-4470-6350
Jifeng ZhangCenter for Advanced Models for Translational Sciences and Therapeutics, University of Michigan Medical Center, Ann Arbor, MI, USA.ORCID 0000-0001-5161-4705
Yuqing Eugene ChenCenter for Advanced Models for Translational Sciences and Therapeutics, University of Michigan Medical Center, Ann Arbor, MI, USA.ORCID 0000-0003-2357-7825
Huijun SunDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Jingyan LiangResearch Center for Vascular Biology, School of Medicine, Yangzhou University, Yangzhou, China.
Jianglin FanDepartment of Molecular Pathology, Faculty of Medicine, Graduate School of Medical Sciences, University of Yamanashi, Yamanashi, Japan.ORCID 0000-0002-1737-6130
University of Michigan · USSaga University · JPUniversity of Yamanashi · JPWuyi University · CNAkita University · JPDalian Medical University · CNMichigan Center for Translational Pathology · USXi'an Jiaotong University · CNYangzhou University · CN

Funding

MPO, HDL Dysfunction and Cardiovascular DiseaseR01HL129778 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2015 to 2018
$2.9M
CETP and HDL Function in Cardiovascular DiseasesR01HL117491 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2013 to 2016
$2.4M
NHLBI NIH HHS R01 HL117491NHLBI NIH HHS R01 HL129778NIH HHS R01HL117491NIH HHS R01HL129778
6 · The paper itself

Abstract

Matrix metalloproteinase-9 (MMP-9), or gelatinase B, has been hypothesized to be involved in the progression of atherosclerosis. In the arterial wall, accumulated macrophages secrete considerable amounts of MMP-9 but its pathophysiological functions in atherosclerosis have not been fully elucidated. To examine the hypothesis that macrophage-derived MMP-9 may affect atherosclerosis, we created MMP-9 transgenic (Tg) rabbits to overexpress the rabbit MMP-9 gene under the control of the scavenger receptor A enhancer/promoter and examined their susceptibility to cholesterol diet-induced atherosclerosis. Tg rabbits along with non-Tg rabbits were fed a cholesterol diet for 16 and 28 weeks, and their aortic and coronary atherosclerosis was compared. Gross aortic lesion areas were significantly increased in female Tg rabbits at 28 weeks; however, pathological examination revealed that all the lesions of Tg rabbits fed a cholesterol diet for either 16 or 28 weeks were characterized by increased monocyte/macrophage accumulation and prominent lipid core formation compared with those of non-Tg rabbits. Macrophages isolated from Tg rabbits exhibited higher infiltrative activity towards a chemoattractant, MCP-1 in vitro and augmented capability of hydrolysing extracellular matrix in granulomatous tissue. Surprisingly, the lesions of Tg rabbits showed more advanced lesions with remarkable calcification in both aortas and coronary arteries. In conclusion, macrophage-derived MMP-9 facilitates the infiltration of monocyte/macrophages into the lesions thereby enhancing the progression of atherosclerosis. Increased accumulation of lesional macrophages may promote vascular calcification.

Indexed as

AnimalsAnimals, Genetically ModifiedAortaCholesterol, DietaryCoronary Artery DiseaseCoronary VesselsDisease Models, AnimalDisease ProgressionHumansMacrophagesMatrix Metalloproteinase 9RabbitsVascular CalcificationCholesterol, DietaryMatrix Metalloproteinase 9atherosclerosiscalcificationhypercholesterolaemiamacrophageMMP-9transgenic rabbits

Identifiers

PMID32126159
PMCPMC7171347
OpenAlexW3010058033

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.