Evidence map›Paper›PMID 23936544›Full record

ArticlePloS one2013

Induction of TGF-β1 synthesis by macrophages in response to apoptotic cells requires activation of the scavenger receptor CD36.

Weipeng Xiong, S Courtney Frasch, Stacey M Thomas, Donna L Bratton, Peter M Henson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.0field-weighted citation impact, top 25% 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, 49 citations in OpenAlex.

  1. Review
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  9. Periosteal CD68Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
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  14. Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis.International journal of molecular sciences · 2021
    Review
  15. Macrophages as a "weapon" in anticancer cellular immunotherapy.The Kaohsiung journal of medical sciences · 2021
    Review
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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

5 authors at 2 institutions in 1 country.

Weipeng XiongDepartment of Pediatrics, National Jewish Health, Denver, Colorado, United States of America.
S Courtney Frasch
Stacey M Thomas
Donna L Bratton
Peter M Henson
University of Colorado Denver · USNational Jewish Health · US

Funding

TRANSLOCATION AND TRANSCELLULAR BIOSYNTHESISP01HL034303 · NHLBI · NATIONAL JEWISH HEALTH · PI BARKLEY, ROBERT · 1985 to 2015
$25.0M
Regulation of Pulmonary InflammationR01HL081151 · NHLBI · NATIONAL JEWISH HEALTH · PI HENSON, PETER M · 2005 to 2012
$3.5M
Apoptosis and defective repair in COPDR01HL088138 · NHLBI · NATIONAL JEWISH HEALTH · PI HENSON, PETER M · 2008 to 2012
$3.5M
Defective PS Exposure in Neutrophil Apoptosis in CGDR01AI058228 · NIAID · NATIONAL JEWISH HEALTH · PI BRATTON, DONNA L · 2004 to 2007
$1.0M
Macrophage PPARg signaling, efferocytosis, and exaggerated inflammation in CGDR56AI058228 · NIAID · NATIONAL JEWISH HEALTH · PI BRATTON, DONNA L · 2011 to 2011
$317k
NHLBI NIH HHS HL034303NHLBI NIH HHS HL081151NHLBI NIH HHS HL088138NHLBI NIH HHS P01 HL034303NHLBI NIH HHS R01 HL081151NHLBI NIH HHS R01 HL088138NIAID NIH HHS AI058228NIAID NIH HHS R01 AI058228NIAID NIH HHS R56 AI058228
6 · The paper itself

Abstract

BACKGROUND/

objectivePhosphatidylserine (PS) exposed on apoptotic cells has been shown to stimulate production of transforming growth factor-β (TGF-β) and promote anti-inflammatory responses. However, the PS receptor(s) responsible for this induction has not been clearly determined. METHODOLOGY/PRINCIPAL

findingsIn the present study, using RAWTβRII cells in which a truncated dominant negative TGF-β receptor II was stably transfected in order to avoid auto-feedback induction of TGF-β, we show that TGF-β1 synthesis is initiated via activation of the scavenger receptor, CD36. The response requires exposure of PS on the apoptotic cell surface and was absent in macrophages lacking CD36. Direct activation of CD36 with an anti-CD36 antibody initiated TGF-β1 production, and signaling pathways involving both Lyn kinase and ERK1/2 were shown to participate in CD36-driven TGF-β1 expression. CONCLUSION/SIGNIFICANCE: Since CD36 has been previously implicated in activation of secreted latent TGF-β, the present study indicates its role in the multiple steps to generation of this important biological mediator.

Indexed as

ApoptosisMAP Kinase Signaling SystemAnimalsBlotting, WesternCD36 AntigensCell ProliferationCells, CulturedEnzyme-Linked Immunosorbent AssayMacrophagesMiceProtein Serine-Threonine KinasesReal-Time Polymerase Chain ReactionReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIReverse Transcriptase Polymerase Chain ReactionRNA, MessengerCD36 Antigenslyn protein-tyrosine kinaseProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIRNA, Messengersrc-Family KinasesTransforming Growth Factor beta1

Identifiers

PMID23936544
PMCPMC3732218
OpenAlexW2018265937

What OpenQuestion holds

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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.