Evidence map›Paper›PMID 24415870›Full record

ArticleWorld journal of gastroenterology2014

Bile acid increases expression of the histamine-producing enzyme, histidine decarboxylase, in gastric cells.

Hye Jin Ku, Hye Young Kim, Hyeong Hoe Kim, Hee Ju Park, Jae Hun Cheong

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Atrazine exposure elicits copy number alterations in the zebrafish genome.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2017
    Article
  8. 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

5 authors at 1 institution in 1 country.

Hye Jin KuHye Jin Ku, Hee Ju Park, Department of Pediatrics, College of Medicine, Pusan National University, Busan 601-721, South Korea.
Hye Young KimHye Jin Ku, Hee Ju Park, Department of Pediatrics, College of Medicine, Pusan National University, Busan 601-721, South Korea.
Hyeong Hoe KimHye Jin Ku, Hee Ju Park, Department of Pediatrics, College of Medicine, Pusan National University, Busan 601-721, South Korea.
Hee Ju ParkHye Jin Ku, Hee Ju Park, Department of Pediatrics, College of Medicine, Pusan National University, Busan 601-721, South Korea.
Jae Hun CheongHye Jin Ku, Hee Ju Park, Department of Pediatrics, College of Medicine, Pusan National University, Busan 601-721, South Korea.
Pusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the effect of bile acid on the expression of histidine decarboxylase (HDC), which is a major enzyme involved in histamine production, and gene expression of gastric transcription factors upon cooperative activation.

methodsHDC expression was examined by immunohistochemistry, reverse transcriptase polymerase chain reaction, and promoter assay in human gastric precancerous tissues, normal stomach tissue, and gastric cancer cell lines. The relationship between gastric precancerous state and HDC expression induced by bile acid was determined. The association between the expression of HDC and various specific transcription factors in gastric cells was also evaluated. MKN45 and AGS human gastric carcinoma cell lines were transfected with farnesoid X receptor (FXR), small heterodimer partner (SHP), and caudal-type homeodomain transcription factor (CDX)1 expression plasmids. The effects of various transcription factors on HDC expression were monitored by luciferase-reporter promoter assay.

resultsHistamine production and secretion in the stomach play critical roles in gastric acid secretion and in the pathogenesis of gastric diseases. Here, we show that bile acid increased the expression of HDC, which is a rate-limiting enzyme of the histamine production pathway. FXR was found to be a primary regulatory transcription factor for bile acid-induced HDC expression. In addition, the transcription factors CDX1 and SHP synergistically enhanced bile acid-induced elevation of HDC gene expression. We confirmed similar expression patterns for HDC, CDX1, and SHP in patient tissues.

conclusionHDC production in the stomach is associated with bile acid exposure and its related transcriptional regulation network of FXR, SHP, and CDX1.

Indexed as

Bile Acids and SaltsCell Line, TumorGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGenes, ReporterHistamineHistidine DecarboxylaseHomeodomain ProteinsHumansMetaplasiaPrecancerous ConditionsPromoter Regions, GeneticReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRNA InterferenceRNA, MessengerBile Acids and SaltsCDX1 protein, humanHistamineHistidine DecarboxylaseHomeodomain Proteinsnuclear receptor subfamily 0, group B, member 2Receptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRNA, MessengerBile acidFarnesoid X receptorHistamineHistidine decarboxylase

Identifiers

PMID24415870
PMCPMC3886006
OpenAlexW1987945448

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.