Evidence map›Paper›PMID 30783144›Full record

ArticleScientific reports2019

A potential peptide derived from cytokine receptors can bind proinflammatory cytokines as a therapeutic strategy for anti-inflammation.

Shinn-Jong Jiang, Pei-I Tsai, Shih-Yi Peng, Chun-Chun Chang, Yi Chung, Hao-Hsiang Tsao, Hsin-Ting Huang, San-Yuan Chen, Hao-Jen Hsu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 34 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 1 country.

Shinn-Jong JiangDepartment of Biochemistry, School of Medicine, Tzu Chi University, Hualien, 97004, Taiwan.
Pei-I TsaiDepartment of Materials Science and Engineering, National Chiao-Tung University, Hsinchu, 30010, Taiwan.ORCID 0000-0002-3516-3120
Shih-Yi PengDepartment of Biochemistry, School of Medicine, Tzu Chi University, Hualien, 97004, Taiwan.
Chun-Chun ChangInstitute of Medical Sciences, Tzu Chi University, Hualien, 97004, Taiwan.
Yi ChungDepartment of Biochemistry, School of Medicine, Tzu Chi University, Hualien, 97004, Taiwan.
Hao-Hsiang TsaoDepartment of Biochemistry, School of Medicine, Tzu Chi University, Hualien, 97004, Taiwan.
Hsin-Ting HuangDepartment of Biochemistry, School of Medicine, Tzu Chi University, Hualien, 97004, Taiwan.
San-Yuan ChenDepartment of Materials Science and Engineering, National Chiao-Tung University, Hsinchu, 30010, Taiwan.
Hao-Jen HsuDepartment of Biochemistry, School of Medicine, Tzu Chi University, Hualien, 97004, Taiwan. hjhsu32@mail.tcu.edu.tw.
Tzu Chi University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation is a pivotal event in the pathogenesis of cardiovascular diseases, including atherosclerosis, restenosis, and coronary artery disease. The efficacy of current treatment or preventive strategies for such inflammation is still inadequate. Thus, new anti-inflammatory strategies are needed. In this study, based on molecular docking and structural analysis, a potential peptide KCF18 with amphiphilic properties (positively charged and hydrophobic residues) derived from the receptors of proinflammatory cytokines was designed to inhibit cytokine-induced inflammatory response. Simulations suggested that KCF18 could bind to cytokines simultaneously, and electrostatic interactions were dominant. Surface plasmon resonance detection showed that KCF18 bound to both tumor necrosis factor-α (TNF-α) and interleukin-6, which is consistent with MM/PBSA binding free energy calculations. The cell experiments showed that KCF18 significantly reduced the binding of proinflammatory cytokines to their cognate receptors, suppressed TNF-α mRNA expression and monocyte binding and transmigration, and alleviated the infiltration of white blood cells in a peritonitis mouse model. The designed peptide KCF18 could remarkably diminish the risk of vascular inflammation by decreasing plasma cytokines release and by directly acting on the vascular endothelium. This study demonstrated that a combination of structure-based in silico design calculations, together with experimental measurements can be used to develop potential anti-inflammatory agents.

Indexed as

HumansInflammationInterleukin-1betaInterleukin-6PeptidesProtein BindingReceptors, CytokineTHP-1 CellsTumor Necrosis Factor-alphaInterleukin-1betaInterleukin-6PeptidesReceptors, CytokineTumor Necrosis Factor-alpha

Identifiers

PMID30783144
PMCPMC6381106
OpenAlexW2911334303

What OpenQuestion holds

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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.