Evidence map›Paper›PMID 25120739›Full record

ArticleInternational journal of clinical and experimental pathology2014

Interleukin-1β induces autophagy by affecting calcium homeostasis and trypsinogen activation in pancreatic acinar cells.

Bin Xu, Bin Bai, Sumei Sha, Pengfei Yu, Yanxin An, Shiqi Wang, Xiangyun Kong, Chaoxu Liu, Ni Wei, Quanxin Feng and 1 more

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Therapeutic Significance of NLRP3 Inflammasome in Cancer: Friend or Foe?International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Changes in cytokines and chemokines in an acute pancreatitis model.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Mogroside IIFrontiers in pharmacology · 2020
    Article
  18. Review
  19. Review
  20. New Advances in the Treatment of Acute Pancreatitis.Current treatment options in gastroenterology · 2019
    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

11 authors at 2 institutions in 1 country.

Bin XuState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Bin BaiState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Sumei ShaState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Pengfei YuState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Yanxin AnState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Shiqi WangState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Xiangyun KongDepartment of Gastroenterology, Xi'an No.1 Hospital Xi'an, Shaanxi Province 710002, China.
Chaoxu LiuState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Ni WeiState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Quanxin FengState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Qingchuan ZhaoState Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, The Fourth Military Medical University 127 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Xijing Hospital · CNWuhan No.1 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The strong up-regulation of inflammatory mediators has been reported to play a key role in acute pancreatitis (AP). Elevated serum levels of interleukin-1β (IL-1β) are associated with the development of AP. However, the precise effect and mechanism of IL-1β in AP remains obscure. In this study, we investigated the potential role and mechanism of IL-1β in AP. We measured autophagy activation in response to IL-1β in AR42J cells. The disrupting effects of IL-1β on cellular Ca(2+) were observed. To determine whether the disruption of Ca(2+) signaling has protective effects in vivo during AP, male C57BL/6 mice were treated with cerulein to induce AP. We found that the treatment of AR42J cells with IL-1β triggered autophagy and that the autophagic flux was impaired. In addition, IL-1β induced Ca(2+) release from the ER. Furthermore, the expression of the ER stress markers GRP78 and IRE1 also increased. 2APB, an antagonist of the InsP3 receptor, inhibited increased expression of autophagy markers. Subsequent biochemical assays revealed that co-culture with IL-1β could induce the activation of trypsinogen to trypsin and reduce the viability of acinar cells. Pathological changes of the pancreas were also observed in vivo. We found that the pathological injuries of the pancreas were significantly alleviated in mice co-treated with 2APB. Taken together, our results indicate that IL-1β can induce trypsin activation and decrease cellular viability in pancreatic acinar cells. These effects depend on impaired autophagy via intracellular calcium changes. Ca(2+) signaling may become a promising therapeutic target in the treatment of pancreatitis.

Indexed as

AutophagyAcinar CellsAnimalsBlotting, WesternCalcium SignalingEndoplasmic Reticulum Chaperone BiPHomeostasisInterleukin-1betaMaleMiceMice, Inbred C57BLMicroscopy, ConfocalMicroscopy, Electron, TransmissionPancreasPancreatitisRatsEndoplasmic Reticulum Chaperone BiPHspa5 protein, mouseInterleukin-1betaTrypsinogenautophagycalciumIL-1βpancreatitis

Identifiers

PMID25120739
PMCPMC4128974
OpenAlexW62230454

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.