Evidence map›Paper›PMID 27002329›Full record

ArticlePloS one2016

Endothelium-Derived 5-Methoxytryptophan Protects Endothelial Barrier Function by Blocking p38 MAPK Activation.

Ling-Yun Chu, Yi-Fu Wang, Huei-Hsuan Cheng, Cheng-Chin Kuo, Kenneth K Wu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

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  13. Characterizing the metabolic response of the zebrafish kidney to overfeeding.American journal of physiology. Renal physiology · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Cytoguardin: A Tryptophan Metabolite against Cancer Growth and Metastasis.International journal of molecular sciences · 2021
    Review
  18. Control of Mesenchymal Stromal Cell Senescence by Tryptophan Metabolites.International journal of molecular sciences · 2021
    Review
  19. Review
  20. 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

5 authors at 3 institutions in 1 country.

Ling-Yun ChuMetabolomic Medicine Research Center, China Medical University Hospital, Taichung, Taiwan.
Yi-Fu WangInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Huei-Hsuan ChengMetabolomic Medicine Research Center, China Medical University Hospital, Taichung, Taiwan.
Cheng-Chin KuoMetabolomic Medicine Research Center, China Medical University Hospital, Taichung, Taiwan.
Kenneth K WuMetabolomic Medicine Research Center, China Medical University Hospital, Taichung, Taiwan.
China Medical University Hospital · TWNational Tsing Hua University · TWNational Health Research Institutes · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endothelial junction is tightly controlled to restrict the passage of blood cells and solutes. Disruption of endothelial barrier function by bacterial endotoxins, cytokines or growth factors results in inflammation and vascular damage leading to vascular diseases. We have identified 5-methoxytryptophan (5-MTP) as an anti-inflammatory factor by metabolomic analysis of conditioned medium of human fibroblasts. Here we postulated that endothelial cells release 5-MTP to protect the barrier function. Conditioned medium of human umbilical vein endothelial cells (HUVECs) prevented endothelial hyperpermeability and VE-cadherin downregulation induced by VEGF, LPS and cytokines. We analyzed the metabolomic profile of HUVEC conditioned medium and detected 5-MTP but not melatonin, serotonin or their catabolites, which was confirmed by enzyme-linked immunosorbent assay. Addition of synthetic pure 5-MTP preserved VE-cadherin and maintained barrier function despite challenge with pro-inflammatory mediators. Tryptophan hydroxylase-1, an enzyme required for 5-MTP biosynthesis, was downregulated in HUVECs by pro-inflammatory mediators and it was accompanied by reduction of 5-MTP. 5-MTP protected VE-cadherin and prevented endothelial hyperpermeability by blocking p38 MAPK activation. A chemical inhibitor of p38 MAPK, SB202190, exhibited a similar protective effect as 5-MTP. To determine whether 5-MTP prevents vascular hyperpermeability in vivo, we evaluated the effect of 5-MTP administration on LPS-induced murine microvascular permeability with Evans blue. 5-MTP significantly prevented Evans blue dye leakage. Our findings indicate that 5-MTP is a new class of endothelium-derived molecules which protects endothelial barrier function by blocking p38 MAPK.

Indexed as

AnimalsAntigens, CDCadherin 5CadherinsCapillary PermeabilityCells, CulturedCulture Media, ConditionedDown-RegulationEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsInflammationMaleMiceMice, Inbred C57BLp38 Mitogen-Activated Protein Kinases5-methoxytryptophanAntigens, CDCadherin 5CadherinsCulture Media, Conditionedp38 Mitogen-Activated Protein KinasesProtective AgentsTryptophan

Identifiers

PMID27002329
PMCPMC4803234
OpenAlexW2312161555

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.