Evidence map›Paper›PMID 25133205›Full record

ArticleTheScientificWorldJournal2014

Plasminogen activator inhibitor-1 regulates LPS induced inflammation in rat macrophages through autophagy activation.

Zhong-Hui Wang, Wei-Ying Ren, Lei Zhu, Li-Juan Hu

Open access · goldAbstract read
In one paragraph

Article in TheScientificWorldJournal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. PAI-1, the Plasminogen System, and Skeletal Muscle.International journal of molecular sciences · 2020
    Review
  8. Article
  9. A critical role for plasminogen in inflammation.The Journal of experimental medicine · 2020
    Review
  10. Article
  11. Article
  12. Molecular biomarkers of Graves' ophthalmopathy.Experimental and molecular pathology · 2019
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Reduced monocyte adhesion to aortae of diabetic plasminogen activator inhibitor-1 knockout mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Article
  18. Review
  19. Review
  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

4 authors at 2 institutions in 1 country.

Zhong-Hui WangDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, No. 180, Feng Lin Road, Shanghai 200032, China.
Wei-Ying RenDepartment of Geriatrics, Zhongshan Hospital, Fudan University, No. 180, Feng Lin Road, Shanghai 200032, China.
Lei ZhuDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, No. 180, Feng Lin Road, Shanghai 200032, China.
Li-Juan HuDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, No. 180, Feng Lin Road, Shanghai 200032, China.
Fudan University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe mechanisms by which plasminogen activator inhibitor-1 (PAI-1) regulates inflammation, especially in acute respiratory distress syndrome (ARDS), are largely unknown.

objectiveTo assess the relationship between PAI-1 and autophagy in inflammatory reactions induced by LPS in rat NR8383 cells.

methodsELISA was used to assess the amounts of TNF-α, IL-1β, and PAI-1 in cell culture supernatants; TLR4, MyD88, PAI-1, LC3, Beclin1, and mTOR protein and mRNA levels were determined by western blot and quantitative RT-PCR, respectively; western blot was used to determine NF-κB protein levels. To further evaluate the role of PAI-1, the PAI-1 gene was downregulated and overexpressed using the siRNA transfection technology and the pCDH-PAI-1, respectively. Finally, the GFP Positive Expression Rate Method was used to determine the rate of GFP-LC3 positive NR8383 cells.

resultsIn LPS-induced NR8383 cells, TNF-α, IL-1β, and PAI-1 expression levels increased remarkably. Upon PAI-1 knockdown, TNF-α, IL-1β, PAI-1, TLR4, MyD88, NF-κB, LC3, and Beclin1 levels were decreased, while mTOR increased. Conversely, overexpression of PAI-1 resulted in increased amounts of TNF-α, IL-1β, PAI-1, TLR4, MyD88, NF-κB, LC3, and Beclin1. However, no significant change was observed in mTOR expression.

conclusionsIn NR8383 cells, PAI-1 contributes in the regulation of LPS-induced inflammation, likely by promoting autophagy.

Indexed as

AutophagyAnimalsApoptosis Regulatory ProteinsBeclin-1Cell LineInflammationInterleukin-1betaLipopolysaccharidesMacrophagesMicrotubule-Associated ProteinsMyeloid Differentiation Factor 88NF-kappa BPlasminogen Activator Inhibitor 1RatsRNA, MessengerToll-Like Receptor 4Anxa3 protein, ratApoptosis Regulatory ProteinsBeclin-1Becn1 protein, ratInterleukin-1betaLipopolysaccharidesMicrotubule-Associated ProteinsMyeloid Differentiation Factor 88NF-kappa BPlasminogen Activator Inhibitor 1RNA, MessengerToll-Like Receptor 4TOR Serine-Threonine KinasesTumor Necrosis Factor-alpha

Identifiers

PMID25133205
PMCPMC4122156
OpenAlexW2108746844

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.