Evidence map›Paper›PMID 32677810›Full record

ArticleClinical and translational gastroenterology2020

Role of the Outer Inflammatory Protein A/Cystine-Glutamate Transporter Pathway in Gastric Mucosal Injury Induced by Helicobacter pylori.

Jie Du, Xiao-Hui Li, Fen Liu, Wen-Qun Li, Zhi-Cheng Gong, Yuan-Jian Li

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational gastroenterology, 2020. 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
1.6field-weighted citation impact, top 16% 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, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Metabolic reprogramming inFrontiers in cellular and infection microbiology · 2025
    Review
  5. Article
  6. Review
  7. Animal Models andJournal of clinical medicine · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Cells · 2020
    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

6 authors at 2 institutions in 1 country.

Jie DuDepartment of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, Hunan, China.
Xiao-Hui LiDepartment of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, Hunan, China.
Fen LiuDepartment of Digestion, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Wen-Qun LiDepartment of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, Hunan, China.
Zhi-Cheng GongDepartment of Pharmacy, Xiangya Hospital of Central South University, Changsha, Hunan, China.
Yuan-Jian LiDepartment of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, Hunan, China.
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionHelicobacter pylori infection is a major cause of gastrointestinal diseases. However, the pathogenesis of gastric mucosal injury by H. pylori remains unclear. Exogenous glutamate supplementation protects against gastric mucosal injury caused by H. pylori. Previously, we showed that aspirin-induced gastric injury is associated with reduction in glutamate release by inhibition of cystine-glutamate transporter (xCT) activity. We hypothesized that the xCT pathway is involved in H. pylori-induced gastric mucosal injury. In this study, we tested the activity of xCT and evaluated the regulatory effect of outer inflammatory protein (Oip) A on xCT in H. pylori-induced gastric mucosal injury.

methodsIn the H. pylori-infected mice and cell lines, the activity of xCT and the regulatory effect of microRNA on xCT were tested, and the effect of OipA from H. pylori on xCT activity was observed.

resultsThe results of in vivo and in vitro experiments showed that H. pylori infection induced gastric mucosal injury. This was accompanied by a reduction in xCT activity, which was attenuated by exogenous glutamate treatment. Furthermore, the expression of miR-30b was upregulated, and miR-30b inhibitors significantly restored xCT activity and gastric mucosal injury caused by H. pylori infection. The OipA, a virulence protein from H. pylori, significantly upregulated the expression levels of miR-30b and inhibited xCT activity. DISCUSSION: OipA plays a significant role in H. pylori-induced gastric mucosal injury, and the effects are mediated by micro30b/xCT pathway.

Indexed as

Amino Acid Transport System y+AnimalsBacterial Outer Membrane ProteinsCell LineDisease Models, AnimalGastric MucosaHelicobacter InfectionsHelicobacter pyloriHumansMaleMiceMicroRNAsSignal TransductionUp-RegulationVirulence FactorsAmino Acid Transport System y+Bacterial Outer Membrane ProteinsMicroRNAsMIRN30b microRNA, mouseOipA protein, Helicobacter pyloriSlc7a11 protein, mouseVirulence Factors

Identifiers

PMID32677810
PMCPMC7263648
OpenAlexW3041217501

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.