Evidence map›Paper›PMID 29367652›Full record

ArticleScientific reports2018

9c11tCLA modulates 11t18:1 and 9t18:1 induced inflammations differently in human umbilical vein endothelial cells.

Jing Li, Sheng-Ben Hu, Yue-Ming He, Cheng-Fei Zhuo, Ruo-Lin Zhou, Fang Chen, Hong-Yan Li, Ze-Yuan Deng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

8 authors at 1 institution in 1 country.

Jing LiState Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China.ORCID http://orcid.org/0000-0002-2271-7761
Sheng-Ben HuState Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China.
Yue-Ming HeState Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China.
Cheng-Fei ZhuoState Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China.
Ruo-Lin ZhouState Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China.
Fang ChenState Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China.
Hong-Yan LiState Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China.
Ze-Yuan DengState Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China. zeyuandeng@hotmail.com.
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial inflammation is recognized as the initial stage of a multistep process leading to coronary heart disease (CHD). Recently, the different effects of industrial trans fatty acids (elaidic acid, 9t18:1) and ruminant trans fatty acids (vaccenic acid, 11t18:1) on CHD have been reported in epidemiological and animal studies, however, the mechanism was not fully studied. Therefore, the objective of this study was to explore the underlying mechanism by which 9t18:1 and 11t18:1 affect human umbilical vein endothelial cells (HUVECs) inflammation. We found that 9c11t-CLA modulated the inflammation of HUVECs induced by 9t18:1 and 11t18:1. Fatty acid composition, pro-inflammatory factors, phosphorylation of MAPKs, and the TLR4 level in HUVECs altered by 11t18:1 induction, collectively suggest that the bio-conversion of 11t18:1 to 9c11tCLA might be the cause why 11t18:1 and 9t18:1 have distinct influences on endothelial injuries. It was concluded that it is biosynthesis of 9c11t CLA from11t18:1, and the modulation of TLR4-MAPK pathway by 9c11t CLA, which at least partially account for the slight effect of 11t18:1 on endothelial inflammation.

Indexed as

BiotransformationCells, CulturedHumansHuman Umbilical Vein Endothelial CellsImmunologic FactorsInflammationLinoleic Acids, ConjugatedMitogen-Activated Protein KinasesOleic AcidOleic AcidsPhosphorylationProtein Processing, Post-TranslationalToll-Like Receptor 411-octadecenoic acidelaidic acidImmunologic FactorsLinoleic Acids, ConjugatedMitogen-Activated Protein KinasesOleic AcidOleic AcidsTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID29367652
PMCPMC5784167
OpenAlexW2806264942

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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.