Evidence map›Paper›PMID 27171144›Full record

ArticlePloS one2016

Perfluorooctanesulfonate Mediates Renal Tubular Cell Apoptosis through PPARgamma Inactivation.

Li-Li Wen, Chien-Yu Lin, Hsiu-Chu Chou, Chih-Cheng Chang, Hau-Yin Lo, Shu-Hui Juan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 3 pooled it
2.4field-weighted citation impact, top 14% 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, 3 syntheses or guidelines pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Ferroptosis in Toxicology: Present and Future.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Association of Combined Per- and Polyfluoroalkyl Substances and Metals with Chronic Kidney Disease.International journal of environmental research and public health · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Article
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  16. Article
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  19. Increased toxicity and retention of perflourooctane sulfonate (PFOS) in humanized CYP2B6-Transgenic mice compared to Cyp2b-null mice is relieved by a high-fat diet (HFD).Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021
    Article
  20. 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

6 authors at 2 institutions in 1 country.

Li-Li WenGraduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan.
Chien-Yu LinDepartment of Internal Medicine, En Chu Kong Hospital, New Taipei City, Taiwan.
Hsiu-Chu ChouGraduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan.
Chih-Cheng ChangGraduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan.
Hau-Yin LoGraduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan.
Shu-Hui JuanGraduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan.
Taipei Medical University · TWEn Chu Kong Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Perfluorinated chemicals (PFCs) are ubiquitously distributed in the environments including stainless pan-coating, raincoat, fire extinguisher, and semiconductor products. The PPAR family has been shown to contribute to the toxic effects of PFCs in thymus, immune and excretory systems. Herein, we demonstrated that perfluorooctanesulfonate (PFOS) caused cell apoptosis through increasing ratio of Bcl-xS/xL, cytosolic cytochrome C, and caspase 3 activation in renal tubular cells (RTCs). In addition, PFOS increased transcription of inflammatory cytokines (i.e., TNFα, ICAM1, and MCP1) by NFκB activation. Conversely, PFOS reduced the mRNA levels of antioxidative enzymes, such as glutathione peroxidase, catalase, and superoxide dismutase, as a result of reduced PPARγ transactivational activity by using reporter and chromatin immuoprecipitation (ChIP) assays. PFOS reduced the protein interaction between PPARγ and PPARγ coactivator-1 alpha (PGC1α) by PPARγ deacetylation through Sirt1 upregulation, of which the binding of PPARγ and PGC1α to a peroxisome proliferator response element (PPRE) in the promoter regions of these antioxidative enzymes was alleviated in the ChIP assay. Furthermore, Sirt1 also deacetylated p53 and then increased the binding of p53 to Bax, resulting in increased cytosolic cytochrome C. The effect of PPARγ inactivation by PFOS was validated using the PPARγ antagonist GW9662, whereas the adverse effects of PFOS were prevented by PPARγ overexpression and activators, rosiglitozone and L-carnitine, in RTCs. The in vitro finding of protective effect of L-carnitine was substantiated in vivo using Balb/c mice model subjected to PFOS challenge. Altogether, we provide in vivo and in vitro evidence for the protective mechanism of L-carnitine in eliminating PFOS-mediated renal injury, at least partially, through PPARγ activation.

Indexed as

AcetylationAlkanesulfonic AcidsAnimalsAntioxidantsApoptosisbcl-2-Associated X ProteinCarnitineCell LineCell ProliferationCytochromes cCytosolFluorocarbonsGenes, ReporterInflammationKidney Function TestsKidney TubulesAlkanesulfonic AcidsAntioxidantsbcl-2-Associated X ProteinCarnitineCytochromes cFluorocarbonsperfluorooctane sulfonic acidPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR gammaProtective AgentsRosiglitazoneSirtuin 1ThiazolidinedionesTumor Suppressor Protein p53

Identifiers

PMID27171144
PMCPMC4865156
OpenAlexW2369268008

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.