Evidence map›Paper›PMID 28898406›Full record

ArticleClinical and experimental immunology2018

DC-SIGN reacts with TLR-4 and regulates inflammatory cytokine expression via NF-κB activation in renal tubular epithelial cells during acute renal injury.

D Feng, Y Wang, Y Liu, L Wu, X Li, Y Chen, Y Chen, Y Chen, C Xu, K Yang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  14. [Quercetin alleviates lipopolysaccharide-induced acute kidney injury in mice by suppressing TLR4/NF-κB pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
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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

11 authors at 1 institution in 1 country.

D FengDepartment of Pediatrics, Ruijin Hospital, Shanghai, China.
Y WangInstitute of Cardiovascular Disease, Ruijin Hospital, Shanghai, China.
Y LiuInstitute of Cardiovascular Disease, Ruijin Hospital, Shanghai, China.
L WuInstitute of Cardiovascular Disease, Ruijin Hospital, Shanghai, China.
X LiDepartment of Nephrology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Y ChenDepartment of Pediatrics, Ruijin Hospital, Shanghai, China.
Y ChenInstitute of Cardiovascular Disease, Ruijin Hospital, Shanghai, China.
Y ChenInstitute of Cardiovascular Disease, Ruijin Hospital, Shanghai, China.
C XuDepartment of Pediatrics, Ruijin Hospital, Shanghai, China.
K YangInstitute of Cardiovascular Disease, Ruijin Hospital, Shanghai, China.
T ZhouDepartment of Pediatrics, Ruijin Hospital, Shanghai, China.ORCID 0000-0002-1178-2613
Ruijin Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the pathological process of acute kidney injury (AKI), innate immune receptors are essential in inflammatory response modulation; however, the precise molecular mechanisms are still unclear. Our study sought to demonstrate the inflammatory response mechanisms in renal tubular epithelial cells via Toll-like receptor-4 (TLR-4) and dendritic cell-specific intercellular adhesion molecule 3-grabbing non-integrin 1 (DC-SIGN) signalling. We found that DC-SIGN exhibited strong expression in renal tubular epithelial cells of human acute renal injury tissues. DC-SIGN protein expression was increased significantly when renal tubular epithelial cells were exposed to lipopolysaccharide (LPS) for a short period. Furthermore, DC-SIGN was involved in the activation of p65 by TLR-4, which excluded p38 and c-Jun N-terminal kinases (JNK). Interleukin (IL)-6 and tumour necrosis factor (TNF)-α expression was decreased after DC-SIGN knock-down, and LPS induced endogenous interactions and plasma membrane co-expression between TLR-4 and DC-SIGN. These results show that DC-SIGN and TLR-4 interactions regulate inflammatory responses in renal tubular epithelial cells and participate in AKI pathogenesis.

Indexed as

Acute Kidney InjuryBiomarkersCell Adhesion MoleculesCell LineCytokinesDC-Specific ICAM-3 Grabbing NonintegrinEpithelial CellsGene ExpressionGene Knockdown TechniquesGene SilencingHumansImmunohistochemistryInflammation MediatorsKidney TubulesLectins, C-TypeMyeloid Differentiation Factor 88BiomarkersCell Adhesion MoleculesCytokinesDC-Specific ICAM-3 Grabbing NonintegrinInflammation MediatorsLectins, C-TypeMyeloid Differentiation Factor 88NF-kappa BReceptors, Cell SurfaceRNA, Small InterferingTLR4 protein, humanToll-Like Receptor 4acute kidney injuryDC-SIGNNF-κBrenal tubular epithelial cellsTLR-4

Identifiers

PMID28898406
PMCPMC5721233
OpenAlexW2755199873

What OpenQuestion holds

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Registered trials

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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.