Evidence map›Paper›PMID 25202989›Full record

ArticlePloS one2014

Upregulation of 5-hydroxytryptamine receptor signaling in coronary arteries after organ culture.

Chun-Yu Deng, Hui Yang, Su-Juan Kuang, Fang Rao, Yu-Mei Xue, Zhi-Ling Zhou, Xiao-Ying Liu, Zhi-Xin Shan, Xiao-Hong Li, Qiu-Xiong Lin and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. PMEnvironmental science and pollution research international · 2022
    Article
  4. 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

12 authors at 2 institutions in 1 country.

Chun-Yu DengMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Hui YangMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Su-Juan KuangMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Fang RaoMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Yu-Mei XueMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Zhi-Ling ZhouMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Xiao-Ying LiuMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Zhi-Xin ShanMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Xiao-Hong LiMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Qiu-Xiong LinMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Shu-Lin WuMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Xi-Yong YuMedical Research Center of Guangdong General Hospital, Guangzhou, P.R. China; Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, P.R. China.
Guangdong Academy of Medical Sciences · CNGuangdong General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background5-Hydroxytryptamine (5-HT) is a powerful constrictor of coronary arteries and is considered to be involved in the pathophysiological mechanisms of coronary-artery spasm. However, the mechanism of enhancement of coronary-artery constriction to 5-HT during the development of coronary artery disease remains to be elucidated. Organ culture of intact blood-vessel segments has been suggested as a model for the phenotypic changes of smooth muscle cells in cardiovascular disease. METHODOLOGY/PRINCIPAL

findingsWe wished to characterize 5-HT receptor-induced vasoconstriction and quantify expression of 5-HT receptor signaling in cultured rat coronary arteries. Cumulative application of 5-HT produced a concentration-dependent vasoconstriction in fresh and 24 h-cultured rat coronary arteries without endothelia. 5-HT induced greater constriction in cultured coronary arteries than in fresh coronary arteries. U46619- and CaCl2-induced constriction in the two groups was comparable. 5-HT stimulates the 5-HT2A receptor and cascade of phospholipase C to induce coronary vasoconstriction. Calcium influx through L-type calcium channels and non-L-type calcium channels contributed to the coronary-artery constrictions induced by 5-HT. The contractions mediated by non-L-type calcium channels were significantly enhanced in cultured coronary arteries compared with fresh coronary arteries. The vasoconstriction induced by thapsigargin was also augmented in cultured coronary arteries. The decrease in Orai1 expression significantly inhibited 5-HT-evoked entry of Ca2+ in coronary artery cells. Expression of the 5-HT2A receptor, Orai1 and STIM1 were augmented in cultured coronary arteries compared with fresh coronary arteries.

conclusionsAn increased contraction in response to 5-HT was mediated by the upregulation of 5-HT2A receptors and downstream signaling in cultured coronary arteries.

Indexed as

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidAnimalsCalciumCalcium ChannelsCalcium Channels, L-TypeCoronary VesselsMaleMembrane GlycoproteinsMuscle, Smooth, VascularMyocytes, Smooth MuscleORAI1 ProteinOrgan Culture TechniquesRatsRats, Sprague-DawleyReceptor, Serotonin, 5-HT2ASerotonin15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidCalciumCalcium ChannelsCalcium Channels, L-TypeMembrane GlycoproteinsORAI1 ProteinOrai1 protein, ratReceptor, Serotonin, 5-HT2ASerotoninStim1 protein, ratStromal Interaction Molecule 1Thapsigargin

Identifiers

PMID25202989
PMCPMC4159325
OpenAlexW1992848727

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.