Evidence map›Paper›PMID 23686433›Full record

ArticleMolecules and cells2013

Angiopoietin-1 elicits pro-inflammatory responses in monocytes and differentiating macrophages.

Seung Hyeok Seok, Jong-Ik Heo, Ji-Hye Hwang, Yi-Rang Na, Jang-Hyuk Yun, Eun Hui Lee, Jong-Wan Park, Chung-Hyun Cho

Abstract read
In one paragraph

Article in Molecules and cells, 2013. 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
1.8field-weighted citation impact, top 16% 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, 36 citations in OpenAlex.

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  15. TREM-1 Attenuates RIPK3-mediated Necroptosis in Hyperoxia-induced Lung Injury in Neonatal Mice.American journal of respiratory cell and molecular biology · 2019
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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

8 authors at 2 institutions in 1 country.

Seung Hyeok SeokDepartment of Microbiology and Immunology and Institute of Endemic Disease, The Catholic University of Korea, Seoul 137-701, Korea.
Jong-Ik Heo
Ji-Hye Hwang
Yi-Rang Na
Jang-Hyuk Yun
Eun Hui Lee
Jong-Wan Park
Chung-Hyun Cho
Seoul National University · KRCatholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The angiopoietin/Tie2 system is an important regulator of angiogenesis and inflammation. In addition to its functions in endothelial cells, Tie2 expression on non-endothelial cells allows for angiopoietin ligands to stimulate the cells. Although Ang1 is a strong Tie2 receptor agonist, little is known regarding the effect of Ang1 on non-endothelial cells, such as monocytes and macrophages. In this study, we found that Ang1 functionally binds to and stimulates monocytes via p38 and Erk1/2 phosphorylation. Ang1-mediated monocyte stimulation is associated with proinflammatory cytokine TNF-α expression. We also determined that Ang1 switched macrophage differentiation toward a pro-inflammatory phenotype, even in the presence of an anti-inflammatory mediator. These findings suggest that Ang1 plays a role in stimulating pro-inflammatory responses and could provide a new strategy by which to manage inflammatory responses.

Indexed as

Angiopoietin-1Cell DifferentiationCell LineEndothelial CellsHumansInflammation MediatorsMacrophagesMAP Kinase Signaling SystemMonocytesNeovascularization, Physiologicp38 Mitogen-Activated Protein KinasesPhosphorylationReceptor, TIE-2Recombinant ProteinsTumor Necrosis Factor-alphaAngiopoietin-1Inflammation Mediatorsp38 Mitogen-Activated Protein KinasesReceptor, TIE-2Recombinant ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID23686433
PMCPMC3887877
OpenAlexW2016679371

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.