Evidence map›Paper›PMID 31856086›Full record

ArticlePancreas2020

Nuclear Factor-κB Increases Intracellular Calcium by Upregulation of Na+-Ca2+ Exchanger 1 in Cerulein-Induced Acute Pancreatitis.

Yuyang Chen, Wanling Li, Rui Xie, Bo Tang, YuFeng Xiao, Feng Yang, Siyuan Chen, Senyuan Yu, Shiming Yang, Hui Dong and 2 more

Open access · greenAbstract read
In one paragraph

Article in Pancreas, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Fibroblast Growth Factor (FGF) Signaling Protects Against Acute Pancreatitis-Induced Damage by Modulating Inflammatory Responses.Medical science monitor : international medical journal of experimental and clinical research · 2020
    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 6 institutions in 3 countries.

Yuyang ChenFrom the Department of Gastroenterology, Xinqiao Hospital, Army Medical University.
Wanling Li
Rui XieDepartment of Gastroenterology, Affiliated Hospital to Zunyi Medical College, Zunyi.
Bo TangFrom the Department of Gastroenterology, Xinqiao Hospital, Army Medical University.
YuFeng XiaoFrom the Department of Gastroenterology, Xinqiao Hospital, Army Medical University.
Feng YangFrom the Department of Gastroenterology, Xinqiao Hospital, Army Medical University.
Siyuan ChenFrom the Department of Gastroenterology, Xinqiao Hospital, Army Medical University.
Senyuan YuDepartment of Gastroenterology, Clinical College of Chinese People's Liberation Army, Anhui Medical University, Hefei, China.
Shiming YangFrom the Department of Gastroenterology, Xinqiao Hospital, Army Medical University.
Hui Dong
Hong GuoFrom the Department of Gastroenterology, Xinqiao Hospital, Army Medical University.
Jing-Jing Liu
Army Medical University · CNXinqiao Hospital · CNAffiliated Hospital of Zunyi Medical College · CNAnhui Medical University · CNChongqing Medical University · CNUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe mechanisms underlying pathogenesis of acute pancreatitis (AP) are still not completely understood. An early, critical feature of AP is aberrant calcium (Ca) signaling, termed Ca overload, within pancreatic acinar cells. This study aimed to develop a model system in rats for AP induction to study the contribution of the Na-Ca exchanger 1 (NCX1) ion channel in AP pathogenesis.

methodsTo establish a rat model of AP induction, cerulein or L-arginine were intraperitoneally injected and tissue was histologically analyzed by hematoxylin and eosin staining. A cell culture-based model for AP induction was similarly created through cerulein treatment of AR42J cells. Induction of AP was also examined following exposure to the NXC1-targeted inhibitor KB-R7943. The expression of each gene was detected by Western blotting, immunofluorescence, immunohistochemistry, or quantitative reverse transcription polymerase chain reaction. Transcriptional regulation by nuclear factor (NF)-κB was detected using an NCX1 promoter-fusion dual luciferase reporter system. Cytosolic Ca was measured using a fluorescent calcium indicator.

resultsWe found that cerulein induced NCX1 expression via activation of nuclear factor NF-κB, which potentially binds to the NCX1 promoter to induce its transcription.

conclusionsOur findings reveal a regulatory pathway through NF-κB/NCX1 governing Ca overload in AP development, thus providing potential targets for AP treatment.

Indexed as

Acinar CellsAcute DiseaseAnimalsCalciumCalcium SignalingCell Line, TumorCeruletideGene Expression RegulationIntracellular SpaceMaleNF-kappa BPancreasPancreatitisRats, Sprague-DawleySodium-Calcium ExchangerUp-RegulationCalciumCeruletideNF-kappa BSodium-Calcium Exchangersodium-calcium exchanger 1

Identifiers

PMID31856086
PMCPMC6946105
OpenAlexW2995919209

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.