Evidence map›Paper›PMID 22596222›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Toll-like receptor 4 activation in microvascular endothelial cells triggers a robust inflammatory response and cross talk with mononuclear cells via interleukin-6.

Zhongyang Lu, Yanchun Li, Junfei Jin, Xiaoming Zhang, Maria F Lopes-Virella, Yan Huang

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

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  6. Sympathetic regulation of the host immune response to bacterial sepsis.Clinical science (London, England : 1979) · 2025
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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

6 authors at 1 institution in 1 country.

Zhongyang LuRalph H. Johnson Veterans Affairs Medical Center, Charleston, SC, USA.
Yanchun Li
Junfei Jin
Xiaoming Zhang
Maria F Lopes-Virella
Yan Huang
Ralph H. Johnson VA Medical Center · US

Funding

The Effect of Statin on Diabetes-Associated Peridontal DiseaseR01DE016353 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HUANG, YAN · 2005 to 2014
$3.3M
Biomarkers of Vascular Disease Progression in Type 1 Diabetes MellitusR01DK081352 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LOPES-VIRELLA, MARIA F · 2008 to 2011
$2.2M
NIDCR NIH HHS DE016353NIDCR NIH HHS R01 DE016353NIDDK NIH HHS DK081352NIDDK NIH HHS R01 DK081352
6 · The paper itself

Abstract

objectiveIt is known that toll-like receptor 4 (TLR4) plays an important role in atherosclerosis. Because both microvascular (MIC) and macrovascular (MAC) endothelial cells (ECs) are present in atherosclerotic lesions, the present study compared TLR4-triggered inflammatory response and cross talk with mononuclear cells between MIC and MAC ECs. METHODS AND

resultsELISA, real-time polymerase chain reaction, and gene expression profiling showed that TLR4 activation by lipopolysaccharide stimulated a much higher expression of inflammatory genes including cytokines, chemokines, growth factors, and adhesion molecules in MIC ECs than MAC ECs. Furthermore, coculture studies showed that TLR4 activation in MIC ECs, but not MAC ECs, induced a cross talk with U937 mononuclear cells through MIC EC-released interleukin-6 to upregulate matrix metalloproteinase-1 expression in U937 cells. To explore molecular mechanisms underlying the different responses to TLR4 activation between MIC and MAC ECs, we showed that MIC ECs had a higher expression of TLR4 and CD14 and a higher TLR4-mediated nuclear factor-kappaB activity than MAC ECs.

conclusionsThe present study showed that TLR4 activation triggers a more robust inflammatory response in MIC ECs than MAC ECs. Given the importance of inflammatory cytokines and matrix metalloproteinases in plaque rupture, MIC ECs may play a key role in plaque destabilization through a TLR4-dependent mechanism.

Indexed as

Cells, CulturedEndothelial CellsHumansInflammationInterleukin-6Lipopolysaccharide ReceptorsLipopolysaccharidesMatrix Metalloproteinase 1MicrovesselsNF-kappa BToll-Like Receptor 4U937 CellsInterleukin-6Lipopolysaccharide ReceptorsLipopolysaccharidesMatrix Metalloproteinase 1NF-kappa BTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID22596222
PMCPMC3384534
OpenAlexW2116676130

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.