Evidence map›Paper›PMID 23053343›Full record

ArticleHeart and vessels2013

Urotensin II promotes the production of LTC4 in rat aortic adventitial fibroblasts through NF-κB-5-LO pathway by p38 MAPK and ERK activations.

Xiao Dong, Xiaojin Ye, Nana Song, Jing Zhao, Beibing Di, Fen Peng, Chaoshu Tang, Wenhui Ding

Abstract read
PubMed Publisher
In one paragraph

Article in Heart and vessels, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Sirtuin 6 attenuates angiotensin II-induced vascular adventitial aging in rat aortae by suppressing the NF-κB pathway.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    Article
  6. Urotensin II promotes secretion of LTBArchives of medical science : AMS · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

8 authors at 3 institutions in 1 country.

Xiao DongDivision of Cardiology, Department of Internal Medicine, Peking University First Hospital, Xishikudajie #8, West District, Beijing, 10034, People's Republic of China.
Xiaojin Ye
Nana Song
Jing Zhao
Beibing Di
Fen Peng
Chaoshu Tang
Wenhui Ding
Peking University · CNPeking University First Hospital · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adventitia is the outer part of the arterial wall where the inflammatory response often occurs. Urotensin II (UII) is a potent vasoconstrictive peptide that also promotes the inflammatory process in patients with cardiovascular disease. Leukotriene C4 (LTC4), a lipid mediator, was recently found to play a role in the inflammatory process in the artery. We hypothesized that the adventitia is one of the resources of LTC4 and that UII may promote LTC4 production through the 5-LO (5-lipoxygenase) pathway in adventitial fibroblasts. Rat adventitial fibroblasts were isolated and incubated in serum-free medium with either UII alone or in combination with inhibitors of p38 MAPK, ERK, and UII receptors. The expression of 5-LO was detected using real-time polymerase chain reaction and Western blot. The translocation and binding activity of nuclear factor (NF)-κB were measured using immunofluorescence and electrophoretic mobility shift assay, respectively. The production of LTC4 was measured by enzyme-linked immunosorbent assay. The results indicated that: (1) adventitial fibroblasts were a source of LTC4 production; (2) UII increased the expression of the 5-LO mRNA and the protein by NF-κB activation through p38 MAPK and ERK pathways; and (3) UII promoted the LTC4 release in fibroblasts through the 5-LO pathway by p38 MAPK and ERK activations. The 5-LO pathway mediates LTC4 production, which may be a new mechanism in the pathogenesis of the vascular adventitial inflammation caused by UII.

Indexed as

Active Transport, Cell NucleusAdventitiaAnimalsAortaArachidonate 5-LipoxygenaseCells, CulturedDose-Response Relationship, DrugEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFibroblastsInflammation MediatorsLeukotriene C4MaleMAP Kinase Signaling SystemNF-kappa Bp38 Mitogen-Activated Protein KinasesArachidonate 5-LipoxygenaseExtracellular Signal-Regulated MAP KinasesInflammation MediatorsLeukotriene C4NF-kappa Bp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsReceptors, G-Protein-CoupledRNA, Messengerurotensin IIUrotensinsUts2r protein, rat

Identifiers

PMID23053343
OpenAlexW2008647965

What OpenQuestion holds

Textmetadata
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.