Evidence map›Paper›PMID 22627090›Full record

ArticleBiochimica et biophysica acta2012

Scavenger receptor A (SR-A) is required for LPS-induced TLR4 mediated NF-κB activation in macrophages.

Honghui Yu, Tuanzhu Ha, Li Liu, Xiaohui Wang, Ming Gao, Jim Kelley, Race Kao, David Williams, Chuanfu Li

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

53 citing papers in PubMed, 96 citations in OpenAlex.

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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

9 authors at 2 institutions in 2 countries.

Honghui YuDepartment of Surgery, James Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Tuanzhu Ha
Li Liu
Xiaohui Wang
Ming Gao
Jim Kelley
Race Kao
David Williams
Chuanfu Li
East Tennessee State University · USJiangsu Province Hospital · CN

Funding

Role of Toll-Like Receptor Signaling in Cardiac IschemiaR01HL071837 · NHLBI · EAST TENNESSEE STATE UNIVERSITY · PI LI, CHUANFU · 2003 to 2022
$6.1M
Innate Immunity and Cardiovascular Function in SepsisR01GM083016 · NIGMS · EAST TENNESSEE STATE UNIVERSITY · PI LI, CHUANFU, WILLIAMS, DAVID L. · 2009 to 2021
$3.8M
Innate Immunity in Trauma HemorrhageR15GM093878 · NIGMS · EAST TENNESSEE STATE UNIVERSITY · PI KAO, RACE L · 2010 to 2010
$422k
NHLBI NIH HHS HL071837NHLBI NIH HHS R01 HL071837NIGMS NIH HHS GM083016NIGMS NIH HHS GM092878NIGMS NIH HHS GM53552NIGMS NIH HHS R01 GM083016NIGMS NIH HHS R15 GM093878
6 · The paper itself

Abstract

Recent evidence suggests that the macrophage scavenger receptor class A (SR-A, aka, CD204) plays a role in the induction of innate immune and inflammatory responses. We investigated whether SR-A will cooperate with Toll-like receptors (TLRs) in response to TLR ligand stimulation. Macrophages (J774/a) were treated with Pam2CSK4, (TLR2 ligand), Polyinosinic:polycytidylic acid (Poly I:C) (TLR3 ligand), and Lipopolysaccharides (LPS) (TLR4 ligand) for 15 min in the presence or absence of fucoidan (the SR-A ligand). The levels of phosphorylated IκBα (p-IκBα) were examined by Western blot. We observed that Poly I:C and LPS alone, but not Pam2CSK4 or fucoidan increased the levels of p-IκBα. However, LPS-induced increases in p-IκBα levels were further enhanced when presence of the fucoidan. Immunoprecipitation and double fluorescent staining showed that LPS stimulation promotes SR-A association with TLR4 in the presence of fucoidan. To further confirm our observation, we isolated peritoneal macrophages from SR-A deficient (SR-A(-/-)), TLR4(-/-) and wild type (WT) mice, respectively. The peritoneal macrophages were treated with LPS for 15min in the presence and absence of fucoidan. We observed that LPS-stimulated TNFα and IL-1β production was further enhanced in the WT macrophages, but did not in either TLR4(-/-) or SR-A(-/-) macrophages, when fucoidan was present. Similarly, in the presence of fucoidan, LPS-induced IκBα phosphorylation, NF-κB binding activity, and association between TLR4 and SR-A were significantly enhanced in WT macrophages compared with LPS stimulation alone. The data suggests that SR-A is needed for LPS-induced inflammatory responses in macrophages.

Indexed as

AnimalsCytokinesDrug SynergismI-kappa B ProteinsInflammation MediatorsLigandsLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLNF-kappa BNF-KappaB Inhibitor alphaPhosphorylationPolysaccharidesProtein BindingScavenger Receptors, Class ACytokinesfucoidanI-kappa B ProteinsInflammation MediatorsLigandsLipopolysaccharidesMsr1 protein, mouseNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, mousePolysaccharidesScavenger Receptors, Class ATlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID22627090
PMCPMC3382073
OpenAlexW2092101871

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.