Evidence map›Paper›PMID 27489164›Full record

ArticleScientific reports2016

Soluble egg antigens of Schistosoma japonicum induce senescence in activated hepatic stellate cells by activation of the STAT3/p53/p21 pathway.

Jinling Chen, Jing Pan, Jianxin Wang, Ke Song, Dandan Zhu, Caiqun Huang, Yinong Duan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 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
3.0field-weighted citation impact, top 8% 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, 30 citations in OpenAlex.

  1. Article
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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

7 authors at 1 institution in 1 country.

Jinling ChenDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong 226001, Jiangsu, People's Republic of China.
Jing PanDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong 226001, Jiangsu, People's Republic of China.
Jianxin WangLaboratory Medicine Center, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, People's Republic of China.
Ke SongOrthopedics and Traumatology Center of PLA, The 153rd Central Hospital of People's Liberation Army, Zhengzhou 450042, Henan, People's Republic of China.
Dandan ZhuDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong 226001, Jiangsu, People's Republic of China.
Caiqun HuangDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong 226001, Jiangsu, People's Republic of China.
Yinong DuanDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong 226001, Jiangsu, People's Republic of China.
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is characterized by the activation of hepatic stellate cells (HSCs). Recent findings suggest that senescence of activated HSCs might limit the development of liver fibrosis. Based on previously observed anti-fibrotic effects of soluble egg antigens from Schistosoma japonicum in vitro, we hypothesized that SEA might play a crucial role in alleviating liver fibrosis through promoting senescence of activated HSCs. We show here that SEA inhibited expression of α-SMA and pro-collagen I and promoted senescence of activated HSCs in vitro. In addition, SEA induced an increased expression of P-p53 and p21. Knockdown of p53 inhibited the expression of p21 and failed to induce senescence of activated-HSCs. Phosphorylated STAT3 was elevated upon SEA stimulation, while loss of STAT3 decreased the level of p53 and senescence of HSCs. Results from immunoprecipitation analysis demonstrated that SOCS3 might be involved in the SEA-induced senescence in HSCs through its interaction with p53. This study demonstrates the potential capacity of SEA in restricting liver fibrosis through promoting senescence in HSCs. Furthermore, a novel STAT3-p53-p21 pathway might participate in the observed SEA-mediated senescence of HSCs. Our results suggest that SEA might carry potential therapeutic effects of restraining liver fibrosis through promoting senescence.

Indexed as

AnimalsAntigens, HelminthCells, CulturedCellular SenescenceCyclin-Dependent Kinase Inhibitor p21Egg ProteinsFibrosisHepatic Stellate CellsLiverMaleMiceMice, Inbred ICRRNA, Small InterferingSchistosoma japonicumSchistosomiasis japonicaSignal TransductionAntigens, HelminthCyclin-Dependent Kinase Inhibitor p21Egg ProteinsRNA, Small InterferingStat3 protein, mouseSTAT3 Transcription FactorTumor Suppressor Protein p53

Identifiers

PMID27489164
PMCPMC4973244
OpenAlexW2484006958

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.