Evidence map›Paper›PMID 25260616›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Regulation of Notch 1 signaling in THP-1 cells enhances M2 macrophage differentiation.

Reetu D Singla, Jing Wang, Dinender K Singla

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

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  9. Transcriptomic Context ofBiomedicines · 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

3 authors at 1 institution in 1 country.

Reetu D SinglaBiomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida.
Jing WangBiomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida.
Dinender K SinglaBiomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida dsingla@ucf.edu.
University of Central Florida · US

Funding

Factors Released From Embryonic Stem cells and Cardiac RemodelingR01HL090646 · NHLBI · UNIVERSITY OF CENTRAL FLORIDA · PI SINGLA, DINENDER KUMAR · 2008 to 2012
$1.8M
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 HL-117241NHLBI NIH HHS R01-HL-090646NHLBI NIH HHS R01-HL-117241
6 · The paper itself

Abstract

Macrophage polarization is emerging as an important area of research for the development of novel therapeutics to treat inflammatory diseases. Within the current study, the role of Notch1R in macrophage differentiation was investigated as well as downstream effects in THP-1 monocytes cultured in "inflammation mimicry" media. Interference of Notch signaling was achieved using either the pharmaceutical inhibitor DAPT or Notch1R small interfering RNA (siRNA), and Notch1R expression, macrophage phenotypes, and anti- and proinflammatory cytokine expression were evaluated. Data presented show that Notch1R expression on M1 macrophages as well as M1 macrophage differentiation is significantly elevated during cellular stress (P < 0.05). However, under identical culture conditions, interference to Notch signaling via Notch1R inhibition mitigated these results as well as promoted M2 macrophage differentiation. Moreover, when subjected to cellular stress, macrophage secretion of proinflammatory cytokines was significantly heightened (P < 0.05). Importantly, Notch1R inhibition not only diminished proinflammatory cytokine secretion but also enhanced anti-inflammatory protein release (P < 0.05). Our data suggest that Notch1R plays a pivotal role in M1 macrophage differentiation and heightened inflammatory responses. Therefore, we conclude that inhibition of Notch1R and subsequent downstream signaling enhances monocyte to M2 polarized macrophage outcomes and promotes anti-inflammatory mediation during cellular stress.

Indexed as

Cell DifferentiationCell LineCell PolarityCulture Media, ConditionedCytokinesHumansInflammation MediatorsMacrophagesMonocytesReceptor, Notch1RNA, Small InterferingSignal TransductionCulture Media, ConditionedCytokinesInflammation MediatorsNOTCH1 protein, humanReceptor, Notch1RNA, Small InterferingatherosclerosismacrophagesmonocytesNotch 1polarization

Identifiers

PMID25260616
PMCPMC4255013
OpenAlexW2123762888

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.