Evidence map›Paper›PMID 24548419›Full record

ArticleCytokine2014

Loss of STAT3 in mouse embryonic fibroblasts reveals its Janus-like actions on mitochondrial function and cell viability.

Fouad A Zouein, Roy J Duhé, Istvan Arany, Kristin Shirey, Jonathan P Hosler, Huiling Liu, Iman Saad, Mazen Kurdi, George W Booz

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cytokine, 2014. 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
1.3field-weighted citation impact, top 20% 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, 21 citations in OpenAlex.

  1. p120-Catenin suppresses NLRP3 inflammasome activation in macrophages.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  2. Single Cell in a Gravity Field.Life (Basel, Switzerland) · 2022
    Review
  3. Article
  4. Article
  5. Mitochondrial Respiration inCurrent issues in molecular biology · 2021
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Mitochondrial Stat3, the Need for Design Thinking.International journal of biological sciences · 2016
    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

9 authors at 3 institutions in 2 countries.

Fouad A ZoueinDepartments of Pharmacology and Toxicology, The University of Mississippi Medical Center, Jackson, MS, USA; School of Medicine and The Mississippi Center for Heart Research, The University of Mississippi Medical Center, Jackson, MS, USA; The Cardiovascular-Renal Research Center, The University of Mississippi Medical Center, Jackson, MS, USA.
Roy J DuhéDepartments of Pharmacology and Toxicology, The University of Mississippi Medical Center, Jackson, MS, USA; Department of Radiation Oncology, The University of Mississippi Medical Center, Jackson, MS, USA; The Cancer Institute, The University of Mississippi Medical Center, Jackson, MS, USA.
Istvan AranyDepartment of Pediatrics, The University of Mississippi Medical Center, Jackson, MS, USA; The Cardiovascular-Renal Research Center, The University of Mississippi Medical Center, Jackson, MS, USA.
Kristin ShireyDepartment of Biochemistry, The University of Mississippi Medical Center, Jackson, MS, USA.
Jonathan P HoslerDepartment of Biochemistry, The University of Mississippi Medical Center, Jackson, MS, USA.
Huiling LiuDepartment of Neurology, The University of Mississippi Medical Center, Jackson, MS, USA.
Iman SaadDepartment of Chemistry and Biochemistry, Faculty of Sciences, Lebanese University, Rafic Hariri Educational Campus, Hadath, Lebanon.
Mazen KurdiDepartments of Pharmacology and Toxicology, The University of Mississippi Medical Center, Jackson, MS, USA; Department of Chemistry and Biochemistry, Faculty of Sciences, Lebanese University, Rafic Hariri Educational Campus, Hadath, Lebanon.
George W BoozDepartments of Pharmacology and Toxicology, The University of Mississippi Medical Center, Jackson, MS, USA; School of Medicine and The Mississippi Center for Heart Research, The University of Mississippi Medical Center, Jackson, MS, USA; The Cardiovascular-Renal Research Center, The University of Mississippi Medical Center, Jackson, MS, USA. Electronic address: gbooz@umc.edu.
University of Mississippi Medical Center · USJackson Memorial Hospital · USLebanese University · LB

Funding

Regulation of IL-6-Type Cytokine Cardioprotective Signaling in the Ischemic HeartR01HL088101 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI BOOZ, GEORGE W. · 2008 to 2012
$2.0M
NHLBI NIH HHS R01 HL088101NHLBI NIH HHS R01HL088101-06
6 · The paper itself

Abstract

STAT3 has been implicated in mitochondrial function; however, the physiological relevance of this action is not established. Here we studied the importance of STAT3 to the cellular response to stimuli, TNFα and serum deprivation, which increase mitochondrial reactive oxygen species (ROS) formation. Experiments were performed using wild type (WT) and STAT3 knockout (KO) mouse embryonic fibroblasts (MEF). Both WT and STAT3 KO MEF expressed similar levels of tumor necrosis factor receptor 1 (TNFR1) and exhibited comparable IκBα degradation with TNFα. However, in the absence of STAT3 nuclear accumulation of NFκB p65 with TNFα was attenuated and induction of the survival protein c-FLIPL was eliminated. Nonetheless, WT MEF were more sensitive to TNFα-induced death which was attributed to necrosis. Deletion of STAT3 decreased ROS formation induced by TNFα and serum deprivation. STAT3 deletion was associated with lower levels of complex I and rates of respiration. Relative to WT cells, mitochondria of STAT3 KO cells released significantly more cytochrome c in response to oxidative stress and had greater caspase 3 cleavage due to serum deprivation. Our findings are consistent with STAT3 being important for mitochondrial function and cell viability by ensuring mitochondrial integrity and the expression of pro-survival genes.

Indexed as

AnimalsCaspase 3Cell NucleusCell RespirationCell SurvivalCytochromes cCytoprotectionEmbryo, MammalianFibroblastsHumansMiceMice, KnockoutMitochondriaModels, BiologicalNF-kappa BProtein BindingCaspase 3Cytochromes cNF-kappa BReactive Oxygen SpeciesStat3 protein, mouseSTAT3 Transcription FactorTumor Necrosis Factor-alphaCell deathMitochondriaNFκBReactive oxygen speciesTumor necrosis factor alpha

Identifiers

PMID24548419
PMCPMC3936345
OpenAlexW1968421845

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.