Evidence map›Paper›PMID 26824441›Full record

ArticlePloS one2016

BMP-7 Treatment Increases M2 Macrophage Differentiation and Reduces Inflammation and Plaque Formation in Apo E-/- Mice.

Dinender K Singla, Reetu Singla, Jing Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.9field-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

50 citing papers in PubMed, 67 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

3 authors at 1 institution in 1 country.

Dinender K SinglaDivision of Metabolic and Cardiovascular Sciences, Biomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL, United States of America.
Reetu SinglaDivision of Metabolic and Cardiovascular Sciences, Biomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL, United States of America.
Jing WangDivision of Metabolic and Cardiovascular Sciences, Biomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL, United States of America.
University of Central Florida · US

Funding

BMP-7 induced Macrophage Polarization in AtherosclerosisR01HL117241 · NHLBI · UNIVERSITY OF CENTRAL FLORIDA · PI PARTHASARATHY, SAMPATH, SINGLA, DINENDER KUMAR · 2013 to 2016
$1.4M
NHLBI NIH HHS R01 HL117241NHLBI NIH HHS R01HL117241
6 · The paper itself

Abstract

Inflammation plays a fundamental role in the inception and development of atherosclerosis (ATH). Mechanisms of inflammation include the infiltration of monocytes into the injured area and subsequent differentiation into either pro-inflammatory M1 macrophages or anti-inflammatory M2 macrophages. We have previously published data suggesting bone morphogenetic protein-7 (BMP-7) enhances M2 macrophage differentiation and anti-inflammatory cytokine secretion in vitro. In this regard, we hypothesized BMP-7 would inhibit plaque formation in an animal model of ATH through monocytic plasticity mediation. ATH was generated in male and female Apo E(-/-) mice via partial left carotid artery (PLCA) ligation and mice were divided into 3 groups: Sham, PLCA, and PLCA+BMP-7 (200 ug/kg; i.v.). Our data suggest that BMP-7 inhibits plaque formation and increases arterial systolic velocity. Furthermore, we report inhibition of monocyte infiltration and a decrease in associated pro-inflammatory cytokines (MCP-1, TNF-α, and IL-6) in the PLCA+BMP-7 mice. In contrast, our data suggest a significant (p<0.05) increase in M2 macrophage populations with consequential enhanced anti-inflammatory cytokine (IL-1RA, IL-10, and Arginase 1) expression following BMP-7 treatment. We have also observed that mechanisms promoting monocyte into M2 macrophage differentiation by BMP-7 involve the upregulation and activation of the BMP-7 receptor (BMP-7RII). In conclusion, we report that BMP-7 has the potential to mediate cellular plasticity and mitigate the inflammatory immune response, which results in decreased plaque formation and improved blood velocity.

Indexed as

AnimalsApolipoproteins EArginaseAtherosclerosisBlood Flow VelocityBone Morphogenetic Protein 7Bone Morphogenetic Protein Receptors, Type IICarotid ArteriesCell DifferentiationChemokine CCL2Disease Models, AnimalFemaleGene Expression RegulationHumansInterleukin-10Interleukin 1 Receptor Antagonist ProteinApolipoproteins EArg1 protein, mouseArginaseBone Morphogenetic Protein 7Bone Morphogenetic Protein Receptors, Type IICcl2 protein, mouseChemokine CCL2IL10 protein, mouseIl1rn protein, mouseInterleukin-10Interleukin 1 Receptor Antagonist ProteinInterleukin-6Protective AgentsTumor Necrosis Factor-alpha

Identifiers

PMID26824441
PMCPMC4732822
OpenAlexW2253234903

What OpenQuestion holds

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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.