Evidence map›Paper›PMID 24975845›Full record

ArticleCellular signalling2014

Prohibitin 1 modulates mitochondrial function of Stat3.

Jie Han, Chunhua Yu, Rhonda F Souza, Arianne L Theiss

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review.International journal of molecular sciences · 2023
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Mitochondrial function and gastrointestinal diseases.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  7. Prohibitions in the meta-inflammatory response: a review.Frontiers in molecular biosciences · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
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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

4 authors at 2 institutions in 1 country.

Jie HanDepartment of Internal Medicine, Division of Gastroenterology, Baylor Research Institute, Baylor University Medical Center, Dallas, TX, United States.
Chunhua YuDepartment of Medicine, Veterans Affairs North Texas Health Care System, University of Texas Southwestern Medical Center, Dallas, TX, United States.
Rhonda F SouzaDepartment of Medicine, Veterans Affairs North Texas Health Care System, University of Texas Southwestern Medical Center, Dallas, TX, United States.
Arianne L TheissDepartment of Internal Medicine, Division of Gastroenterology, Baylor Research Institute, Baylor University Medical Center, Dallas, TX, United States. Electronic address: arianne.theiss@baylorhealth.edu.
Baylor University Medical Center · USVA North Texas Health Care System · US

Funding

Role and function of prohibitin in intestinal inflammationK01DK085222 · NIDDK · EMORY UNIVERSITY · PI THEISS, ARIANNE L · 2010 to 2014
$671k
Maintenance of intestinal epithelial cell homeostasis by prohibitinR03DK098229 · NIDDK · BAYLOR RESEARCH INSTITUTE · PI THEISS, ARIANNE L · 2013 to 2014
$157k
NIDDK NIH HHS K01 DK085222NIDDK NIH HHS K01-DK085222NIDDK NIH HHS R03 DK098229NIDDK NIH HHS R03-DK098229
6 · The paper itself

Abstract

Mitochondrial dysfunction in intestinal epithelial cells (IEC) is thought to precede the onset of inflammatory bowel diseases (IBD). Expression of Prohibitin 1 (PHB), a mitochondrial protein required for optimal electron transport chain (ETC) activity, is decreased in mucosal biopsies during active and inactive IBD. In addition to its activities as a transcription factor, Signal Transducer and Activator of Transcription 3 (Stat3) resides in the mitochondria of cells where phosphorylation at S727 is required for optimal ETC activity and protects against stress-induced mitochondrial dysfunction. Here, we show that PHB overexpression protects against mitochondrial stress and apoptosis of cultured IECs induced by TNFα, which is a pro-inflammatory cytokine involved in IBD pathogenesis. Expression of pS727-Stat3 dominant negative eliminates protection by PHB against TNFα-induced mitochondrial stress and apoptosis. PHB interacts with pS727-Stat3 in the mitochondria of cultured IECs and in colonic epithelium from wild-type mice. Our data suggest a protective role of PHB that is dependent on pS727-Stat3 to prevent mitochondrial dysfunction in IECs. Reduced levels of PHB during IBD may be an underlying factor promoting mitochondrial dysfunction of the intestinal epithelium.

Indexed as

AnimalsApoptosisCaco-2 CellsCells, CulturedEpithelial CellsHumansIntestinal MucosaMiceMice, Inbred C57BLMitochondriaPhosphorylationProhibitinsProtein BindingReactive Oxygen SpeciesRepressor ProteinsSTAT3 Transcription FactorPHB protein, humanProhibitinsReactive Oxygen SpeciesRepressor ProteinsSTAT3 Transcription FactorTumor Necrosis Factor-alphaElectron transport chainIntestinal epitheliumMitochondriaOxidative stressProhibitinStat3

Identifiers

PMID24975845
PMCPMC4130792
OpenAlexW2068041059

What OpenQuestion holds

Textmetadata
LicenceTDM
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.