Evidence map›Paper›PMID 32141127›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Protein S-glutathionylation stimulate adipogenesis by stabilizing C/EBPβ in 3T3L1 cells.

Yosuke Watanabe, Kazuhiro Watanabe, Daisuke Fujioka, Kazuto Nakamura, Takamitsu Nakamura, Manabu Uematsu, Markus M Bachschmid, Reiko Matsui, Kiyotaka Kugiyama

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Regulation of GlutathioneInternational journal of molecular sciences · 2024
    Article
  5. Article
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  8. Review
  9. Review
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  11. Article
  12. Article
  13. Article
  14. Article
  15. Role of Glutaredoxin-1 and Glutathionylation in Cardiovascular Diseases.International journal of molecular sciences · 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

9 authors at 2 institutions in 2 countries.

Yosuke WatanabeDepartment of Internal Medicine II, University of Yamanashi, Chuo, Japan.
Kazuhiro WatanabeDepartment of Internal Medicine II, University of Yamanashi, Chuo, Japan.
Daisuke FujiokaDepartment of Internal Medicine II, University of Yamanashi, Chuo, Japan.
Kazuto NakamuraDepartment of Internal Medicine II, University of Yamanashi, Chuo, Japan.
Takamitsu NakamuraDepartment of Internal Medicine II, University of Yamanashi, Chuo, Japan.
Manabu UematsuDepartment of Internal Medicine II, University of Yamanashi, Chuo, Japan.
Markus M BachschmidDepartment of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Reiko MatsuiDepartment of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Kiyotaka KugiyamaDepartment of Internal Medicine II, University of Yamanashi, Chuo, Japan.
University of Yamanashi · JPBoston University · US

Funding

Redox Control of Hepatic Lipid MetabolismR01DK103750 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BACHSCHMID, MARKUS MICHAEL · 2015 to 2019
$1.8M
Regulation of ischemic limb vascularization by glutaredoxin-1R01HL133013 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MATSUI, REIKO · 2016 to 2019
$1.6M
NHLBI NIH HHS R01 HL133013NIDDK NIH HHS R01 DK103750
6 · The paper itself

Abstract

Reactive oxygen species (ROS) increase during adipogenesis and in obesity. Oxidants react with cysteine residues of proteins to form glutathione (GSH) adducts, S-glutathionylation, that are selectively removed by glutaredoxin-1 (Glrx). We have previously reported that Glrx knockout mice had increased protein S-glutathionylation and developed obesity by an unknown mechanism. In this study, we demonstrated that 3T3L1 adipocytes differentiation increased ROS and protein S-glutathionylation. Glrx ablation elevated protein S-glutathionylation and lipid content in 3T3L1 cells. Glrx replenishment decreased the lipid content of Glrx KO 3T3L1 cells. Glrx KO also increased protein expression and protein S-glutathionylation of the adipogenic transcription factor CCAAT enhancer-binding protein (C/EBP) β. Protein S-glutathionylation decreased the interaction of C/EBPβ and protein inhibitor of activated STAT (PIAS) 1, a small ubiquitin-related modifier E3 ligase that facilitates C/EBPβ degradation. Experiments with truncated mutant C/EBPβ demonstrated that PIAS1 interacted with the liver-enriched inhibitory protein (LIP) region of C/EBPβ. Furthermore, mass spectrometry analysis identified protein S-glutathionylation of Cys201 and Cys296 in the LIP region of C/EBPβ. The C201S, C296S double-mutant C/EBPβ prevented protein S-glutathionylation and preserved the interaction with PIAS1. In summary, Glrx ablation stimulated 3T3L1 cell differentiation and adipogenesis via increased protein S-glutathionylation of C/EBPβ, stabilizing and increasing C/EBPβ protein levels.

Indexed as

AdipogenesisGene Expression Regulation3T3-L1 CellsAdipocytesAnimalsCCAAT-Enhancer-Binding Protein-betaGlutaredoxinsGlutathioneMiceMice, KnockoutProtein Processing, Post-TranslationalProtein SCCAAT-Enhancer-Binding Protein-betaCebpb protein, mouseGlrx protein, mouseGlutaredoxinsGlutathioneProtein SCCAAT enhancer-binding proteinglutaredoxin-1reactive oxygen speciesS-glutathionylation

Identifiers

PMID32141127
PMCPMC8491561
OpenAlexW3010365138

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.