Evidence map›Paper›PMID 28878285›Full record

ArticleScientific reports2017

Interleukin-33 promotes inflammation-induced lymphangiogenesis via ST2/TRAF6-mediated Akt/eNOS/NO signalling pathway.

Longhui Han, Minglian Zhang, Xu Liang, Xin Jia, Jinchen Jia, Miying Zhao, Yiming Fan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Observational
  3. Article
  4. IL-33 Signaling Inhibition Leads to a Preeclampsia-Like Phenotype in Pregnant Rats.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Factors associated with cardiac allograft vasculopathy after heart transplantation.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2022
    Article
  11. Article
  12. The Paradigm Change of IL-33 in Vascular Biology.International journal of molecular sciences · 2021
    Review
  13. Observational
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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

7 authors at 2 institutions in 1 country.

Longhui HanHebei Provincial Key Laboratory of Ophthalmology, Hebei Provincial Eye institute, Hebei Provincial Eye Hospital, Xingtai, Hebei, 054001, China. han-longhui@163.com.
Minglian ZhangHebei Provincial Key Laboratory of Ophthalmology, Hebei Provincial Eye institute, Hebei Provincial Eye Hospital, Xingtai, Hebei, 054001, China. zhmlyk@sohu.com.
Xu LiangTianjin Eye Hospital, Tianjin, 300020, China.
Xin JiaHebei Provincial Key Laboratory of Ophthalmology, Hebei Provincial Eye institute, Hebei Provincial Eye Hospital, Xingtai, Hebei, 054001, China.
Jinchen JiaHebei Provincial Key Laboratory of Ophthalmology, Hebei Provincial Eye institute, Hebei Provincial Eye Hospital, Xingtai, Hebei, 054001, China.
Miying ZhaoHebei Provincial Key Laboratory of Ophthalmology, Hebei Provincial Eye institute, Hebei Provincial Eye Hospital, Xingtai, Hebei, 054001, China.
Yiming FanHebei Provincial Key Laboratory of Ophthalmology, Hebei Provincial Eye institute, Hebei Provincial Eye Hospital, Xingtai, Hebei, 054001, China.
Hebei Eye Hospital · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interplay between inflammation and lymphangiogenesis is mediated by various cytokines. However, most of these molecules and their associated mechanism are yet to be defined. Here, we explored the role of IL-33 in modulating inflammation-induced lymphangiogenesis (ILA) and its underlying mechanisms using an ILA mouse model and a lymphatic endothelial cell (LEC) line. Our results show that IL-33 promoted the proliferation, migration and tube formation of LECs and ILA in vivo. The pro-lymphangiogenic activity of IL-33 was abolished by ST2 blockage. In mechanisms, IL-33 induced the phosphorylation of Akt/eNOS to produce NO in LECs. The IL-33-induced Akt/eNOS activation was suppressed by the PI3K-specific-inhibitor wortmannin, and NO-production was inhibited by both wortmannin and the NO synthase-inhibitor NMA. Knock-down of ST2 or TRAF6 suppressed Akt/eNOS phosphorylation and NO production. The reduction of NO treated with wortmannin or NMA abolished the promoting effects of IL-33 on the chemotactic motility and tube formation of HDLECs. In vivo, IL-33-induced ILA was also impaired in eNOS

Indexed as

LymphangiogenesisSignal TransductionAnimalsBiomarkersCell MovementCell ProliferationCorneaDisease Models, AnimalEndothelial CellsImmunohistochemistryInflammationInterleukin-1 Receptor-Like 1 ProteinInterleukin-33MaleMiceMice, KnockoutBiomarkersIl1rl1 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Nitric OxideNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktTNF Receptor-Associated Factor 6

Identifiers

PMID28878285
PMCPMC5587532
OpenAlexW2751653897

What OpenQuestion holds

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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.