Evidence map›Paper›PMID 28358333›Full record

ArticleSensors (Basel, Switzerland)2017

RAGE Plays a Role in LPS-Induced NF-κB Activation and Endothelial Hyperpermeability.

Liqun Wang, Jie Wu, Xiaohua Guo, Xuliang Huang, Qiaobing Huang

Open access · goldAbstract read
In one paragraph

Article in Sensors (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.4field-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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  19. Molecular Characteristics of RAGE and Advances in Small-Molecule Inhibitors.International journal of molecular sciences · 2021
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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.

Liqun WangDrug Discovery Research Center, Southwest Medical University, 319 Zhongshan Road, Luzhou 646000, China. liqunwang@swmu.edu.cn.
Jie WuFirst Clinical College of Medicine, Southern Medical University, Guangzhou 510515, China. wujie11@smu.edu.cn.
Xiaohua GuoDepartment of Pathophysiology, Key Lab for Shock and Microcirculation Research, Southern Medical University, Guangzhou 510515, China. lanblue@smu.edu.cn.
Xuliang HuangDepartment of Pathophysiology, Key Lab for Shock and Microcirculation Research, Southern Medical University, Guangzhou 510515, China. shock@smu.edu.cn.
Qiaobing HuangDepartment of Pathophysiology, Key Lab for Shock and Microcirculation Research, Southern Medical University, Guangzhou 510515, China. bing@smu.edu.cn.
Southern Medical University · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial functional dysregulation and barrier disruption contribute to the initiation and development of sepsis. The receptor for advanced glycation end products (RAGE) has been demonstrated to be involved in the pathogenesis of sepsis. The present study aimed to investigate the role of RAGE in lipopolysaccharide (LPS)-induced nuclear factor-κB (NF-κB) activation in endothelial cells and the consequent endothelial hyperpermeability. LPS-induced upregulation of RAGE protein expression in human umbilical vein endothelial cells (HUVECs) was detected by western blotting. Activation of NF-κB was revealed using western blotting and immunofluorescent staining. LPS-elicited endothelial hyperpermeability was explored by transendothelial electrical resistance (TER) assay and endothelial monolayer permeability assay. The blocking antibody specific to RAGE was used to confirm the role of RAGE in LPS-mediated NF-κB activation and endothelial barrier disruption. We found that LPS upregulated the protein expression of RAGE in a dose- and time-dependent manner in HUVECs. Moreover, LPS triggered a significant phosphorylation and degradation of IκBα, as well as NF-κB p65 nuclear translocation. Moreover, we observed a significant increase in endothelial permeability after LPS treatment. However, the RAGE blocking antibody attenuated LPS-evoked NF-κB activation and endothelial hyperpermeability. Our results suggest that RAGE plays an important role in LPS-induced NF-κB activation and endothelial barrier dysfunction.

Indexed as

Cells, CulturedHumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesNF-kappa BPhosphorylationReceptor for Advanced Glycation End ProductsLipopolysaccharidesNF-kappa BReceptor for Advanced Glycation End Productsendothelial hyperpermeabilityLPSNF-κBRAGE

Identifiers

PMID28358333
PMCPMC5421682
OpenAlexW2601243565

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.