Evidence map›Paper›PMID 28036393›Full record

ArticlePLoS neglected tropical diseases2016

Soluble Egg Antigens of Schistosoma japonicum Induce Senescence of Activated Hepatic Stellate Cells by Activation of the FoxO3a/SKP2/P27 Pathway.

Yinong Duan, Jing Pan, Jinling Chen, Dandan Zhu, Jianxin Wang, Xiaolei Sun, Liuting Chen, Liting Wu

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-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

16 citing papers in PubMed, 20 citations in OpenAlex.

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  8. Sja-miR-71a inJournal of extracellular vesicles · 2020
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  14. TLR3 Modulates the Response of NK Cells againstJournal of immunology research · 2018
    Article
  15. Hepatic stellate cells as key target in liver fibrosis.Advanced drug delivery reviews · 2017
    Review
  16. 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

8 authors at 1 institution in 1 country.

Yinong DuanDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.ORCID 0000-0001-5824-5762
Jing PanDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Jinling ChenDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Dandan ZhuDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Jianxin WangLaboratory Medicine Center, Affiliated Hospital of Nantong University, Nantong, Jiangsu, People's Republic of China.
Xiaolei SunDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Liuting ChenDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Liting WuDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLiver fibrosis was viewed as a reversible process. The activation of hepatic stellate cells (HSCs) is a key event in the process of liver fibrosis. The induction of senescence of HSCs would accelerate the clearance of the activated HSCs. Previously, we demonstrated that soluble egg antigens (SEA) of Schistosoma japonicum promoted the senescence of HSCs via STAT3/P53/P21 pathway. In this paper, our study was aimed to explore whether there are other signaling pathways in the process of SEA-induced HSCs aging and the underlying effect of SKP2/P27 signal on senescent HSCs. METHODOLOGY/PRINCIPAL

findingsHuman hepatic stellate cell line, LX-2 cells, were cultured and stimulated with SEA. Western blot and cellular immunofluorescence analysis were performed to determine the expression of senescence-associated protein, such as P27, SKP2 and FoxO3a. Besides, RNA interfering was applied to knockdown the expression of related protein. The senescence of HSCs was determined by senescence-associated β-gal staining. We found that SEA increased the expression of P27 protein, whereas it inhibited the expression of SKP2 and FoxO3a. Knockdown of P27 as well as overexpression of SKP2 both suppressed the SEA-induced senescence of HSCs. In addition, the nuclear translocation of FoxO3a from the nucleus to the cytoplasm was induced by SEA stimulation. CONCLUSIONS/SIGNIFICANCE: The present study demonstrates that SEA promotes HSCs senescence through the FoxO3a/SKP2/P27 pathway.

Indexed as

Cellular SenescenceSignal TransductionActive Transport, Cell NucleusAnimalsAntigens, HelminthCell LineCyclin-Dependent Kinase Inhibitor p27EggsForkhead Box Protein O3Hepatic Stellate CellsHumansRNA InterferenceSchistosoma japonicumSolubilityS-Phase Kinase-Associated ProteinsAntigens, HelminthCyclin-Dependent Kinase Inhibitor p27Forkhead Box Protein O3FOXO3 protein, humanS-Phase Kinase-Associated Proteins

Identifiers

PMID28036393
PMCPMC5231384
OpenAlexW2567079628

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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.