Evidence map›Paper›PMID 19850892›Full record

ArticleThe American journal of pathology2009

Suppression of PLCbeta2 by endotoxin plays a role in the adenosine A(2A) receptor-mediated switch of macrophages from an inflammatory to an angiogenic phenotype.

Stan Grinberg, Gyorgy Hasko, Dianqing Wu, Samuel Joseph Leibovich

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.2field-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

57 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
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  6. Macrophage Phenotyping in Atherosclerosis by Proteomics.International journal of molecular sciences · 2023
    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

4 authors at 2 institutions in 1 country.

Stan GrinbergDepartment of Cell Biology and Molecular Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey 07103, USA.
Gyorgy Hasko
Dianqing Wu
Samuel Joseph Leibovich
Rutgers New Jersey Medical SchoolYale University · US

Funding

Integrative Mechanisms in Cardiovascular DiseaseT32HL069752 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 2004 to 2013
$2.9M
Molecular Function of Chemoattractant-Mediated SignalingR01HL080706 · NHLBI · YALE UNIVERSITY · PI WU, DIANQING · 2005 to 2009
$2.3M
Molecular Function of Chemoattractant-Mediated SignalingR01GM054597 · NIGMS · UNIVERSITY OF ROCHESTER · PI WU, DIANQING · 1996 to 2004
$1.2M
NHLBI NIH HHS 5 T32 HL069752NHLBI NIH HHS R01 HL080706NHLBI NIH HHS T32 HL069752NIGMS NIH HHS R01 GM054597NIGMS NIH HHS R01GM06836
6 · The paper itself

Abstract

Toll-like receptor (TLR) 2, 4, 7, and 9 agonists, together with adenosine A(2A) receptor (A(2A)R) agonists, switch macrophages from an inflammatory (M1) to an angiogenic (M2-like) phenotype. This switch involves induction of A(2A)Rs by TLR agonists, down-regulation of tumor necrosis factor alpha (TNFalpha) and interleukin-12, and up-regulation of vascular endothelial growth factor (VEGF) and interleukin-10 expression. We show here that the TLR4 agonist lipopolysaccharide (LPS) induces rapid and specific post-transcriptional down-regulation of phospholipase C(PLC)beta1 and beta2 expression in macrophages by de-stabilizing their mRNAs. The PLCbeta inhibitor U73122 down-regulates TNFalpha expression by macrophages, and in the presence of A(2A)R agonists, up-regulates VEGF, mimicking the synergistic action of LPS with A(2A)R agonists. Selective down-regulation of PLCbeta2, but not PLCbeta1, using small-interfering RNA resulted in increased VEGF expression in response to A(2A)R agonists, but did not suppress TNFalpha expression. Macrophages from PLCbeta2(-/-) mice also expressed increased VEGF in response to A(2A)R agonists. LPS-mediated suppression of PLCbeta1 and beta2 is MyD88-dependent. In a model of endotoxic shock, LPS (35 microg/mouse, i.p.) suppressed PLCbeta1 and beta2 expression in spleen, liver, and lung of wild-type but not MyD88(-/-) mice. These studies indicate that LPS suppresses PLCbeta1 and beta2 expression in macrophages in vitro and in several tissues in vivo. These results suggest that suppression of PLCbeta2 plays an important role in switching M1 macrophages into an M2-like state.

Indexed as

AnimalsBlotting, WesternImmunoprecipitationInflammationIsoenzymesLipopolysaccharidesMacrophage ActivationMacrophagesMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88Neovascularization, PhysiologicPhenotypePhospholipase C betaReceptor, Adenosine A2AIsoenzymesLipopolysaccharidesMyd88 protein, mouseMyeloid Differentiation Factor 88Phospholipase C betaPlcb2 protein, mouseReceptor, Adenosine A2ARNA, Small InterferingTumor Necrosis Factor-alphaVascular Endothelial Growth Factor A

Identifiers

PMID19850892
PMCPMC2789640
OpenAlexW2158530794

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.