Evidence map›Paper›PMID 20574008›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

sRAGE induces human monocyte survival and differentiation.

Yijie Wang, Hongmei Wang, Melissa G Piper, Sara McMaken, Xiaokui Mo, Judy Opalek, Ann Marie Schmidt, Clay B Marsh

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 82 citations in OpenAlex.

  1. Trial
  2. Hyperglycemia, receptor for advanced glycation end products, and small airways dysfunction in asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2026
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  16. Skewed Signaling through the Receptor for Advanced Glycation End-Products Alters the Proinflammatory Profile of Tumor-Associated Macrophages.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2018
    Review
  17. Article
  18. Article
  19. 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

8 authors at 3 institutions in 2 countries.

Yijie WangDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA.
Hongmei Wang
Melissa G Piper
Sara McMaken
Xiaokui Mo
Judy Opalek
Ann Marie Schmidt
Clay B Marsh
The Ohio State University · USSacred Heart Hospital · IEColumbia University Irving Medical Center · US

Funding

NF-kappaB:an Akt target &regulator of monocyte survivalR01HL067176 · NHLBI · OHIO STATE UNIVERSITY · PI MARSH, CLAY B · 2001 to 2011
$3.2M
The role of the miR-17-92 microRNA cluster in the pathogenesis of IPFR01HL102464 · NHLBI · OHIO STATE UNIVERSITY · PI MARSH, CLAY B · 2010 to 2013
$1.5M
NHLBI NIH HHS R01 HL067176NHLBI NIH HHS R01 HL102464
6 · The paper itself

Abstract

The receptor for advanced glycation end products (RAGE) is produced either as a transmembrane or soluble form (sRAGE). Substantial evidence supports a role for RAGE and its ligands in disease. sRAGE is reported to be a competitive, negative regulator of membrane RAGE activation, inhibiting ligand binding. However, some reports indicate that sRAGE is associated with inflammatory disease. We sought to define the biological function of sRAGE on inflammatory cell recruitment, survival, and differentiation in vivo and in vitro. To test the in vivo impact of sRAGE, the recombinant protein was intratracheally administered to mice, which demonstrated monocyte- and neutrophil-mediated lung inflammation. We also observed that sRAGE induced human monocyte and neutrophil migration in vitro. Human monocytes treated with sRAGE produced proinflammatory cytokines and chemokines. Our data demonstrated that sRAGE directly bound human monocytes and monocyte-derived macrophages. Binding of sRAGE to monocytes promoted their survival and differentiation to macrophages. Furthermore, sRAGE binding to cells increased during maturation, which was similar in freshly isolated mouse monocytes compared with mature tissue macrophages. Because sRAGE activated cell survival and differentiation, we examined intracellular pathways that were activated by sRAGE. In primary human monocytes and macrophages, sRAGE treatment activated Akt, Erk, and NF-kappaB, and their activation appeared to be critical for cell survival and differentiation. Our data suggest a novel role for sRAGE in monocyte- and neutrophil-mediated inflammation and mononuclear phagocyte survival and differentiation.

Indexed as

AnimalsCaspase 3Caspase InhibitorsCell AdhesionCell DifferentiationCell Line, TumorCell SurvivalDown-RegulationExtracellular Signal-Regulated MAP KinasesGlycation End Products, AdvancedHumansInflammation MediatorsMacrophages, AlveolarMiceMice, Inbred C57BLMonocytesCASP3 protein, humanCaspase 3Caspase InhibitorsExtracellular Signal-Regulated MAP KinasesGlycation End Products, AdvancedInflammation MediatorsNF-kappa BProto-Oncogene Proteins c-aktReceptor for Advanced Glycation End ProductsReceptors, Immunologic

Identifiers

PMID20574008
PMCPMC3671884
OpenAlexW1946370590

What OpenQuestion holds

Textmetadata
LicenceTDM
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.