Evidence map›Paper›PMID 26878911›Full record

ArticleScientific reports2016

Transcriptional activation of follistatin by Nrf2 protects pulmonary epithelial cells against silica nanoparticle-induced oxidative stress.

Chen Lin, Xinyuan Zhao, Desen Sun, Lingda Zhang, Wenpan Fang, Tingjia Zhu, Qiang Wang, Botao Liu, Saisai Wei, Guangdi Chen and 2 more

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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.7field-weighted citation impact, top 7% 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, 46 citations in OpenAlex.

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  16. STAT3 Partly Inhibits Cell ProliferationFrontiers in genetics · 2021
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  20. Cardiovascular Disease-Related Serum Proteins in Workers Occupationally Exposed to Polycyclic Aromatic Hydrocarbons.Toxicological sciences : an official journal of the Society of Toxicology · 2019
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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

12 authors at 2 institutions in 2 countries.

Chen LinInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Xinyuan ZhaoInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Desen SunInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Lingda ZhangInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Wenpan FangInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Tingjia ZhuInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Qiang WangInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Botao LiuUniversity of Massachusetts Medical School, Program in Molecular Medicine, Worcester, MA, 01605, USA.
Saisai WeiProgram in Molecular Cell Biology, Zhejiang University School of Medicine, Hangzhou, China.
Guangdi ChenInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Zhengping XuInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Xiangwei GaoInstitute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Zhejiang University · CNUniversity of Massachusetts Chan Medical School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Silica nanoparticles (SiO2 NPs) cause oxidative stress in respiratory system. Meanwhile, human cells launch adaptive responses to overcome SiO2 NP toxicity. However, besides a few examples, the regulation of SiO2 NP-responsive proteins and their functions in SiO2 NP response remain largely unknown. In this study, we demonstrated that SiO2 NP induced the expression of follistatin (FST), a stress responsive gene, in mouse lung tissue as well as in human lung epithelial cells (A549). The levels of Ac-H3(K9/18) and H3K4me2, two active gene markers, at FST promoter region were significantly increased during SiO2 NP treatment. The induction of FST transcription was mediated by the nuclear factor erythroid 2-related factor 2 (Nrf2), as evidenced by the decreased FST expression in Nrf2-deficient cells and the direct binding of Nrf2 to FST promoter region. Down-regulation of FST promoted SiO2 NP-induced apoptosis both in cultured cells and in mouse lung tissue. Furthermore, knockdown of FST increased while overexpression of FST decreased the expression level of NADPH oxidase 1 (NOX1) and NOX5 as well as the production of cellular reactive oxygen species (ROS). Taken together, these findings demonstrated a protective role of FST in SiO2 NP-induced oxidative stress and shed light on the interaction between SiO2 NPs and biological systems.

Indexed as

NanoparticlesOxidative StressSilicon DioxideTranscriptional ActivationAlveolar Epithelial CellsAnimalsApoptosisCell LineFollistatinGene ExpressionHumansMaleMembrane ProteinsMiceNADPH Oxidase 1NADPH Oxidase 5FollistatinMembrane ProteinsNADPH Oxidase 1NADPH Oxidase 5NADPH OxidasesNF-E2-Related Factor 2NOX1 protein, humanNOX5 protein, humanReactive Oxygen SpeciesSilicon Dioxide

Identifiers

PMID26878911
PMCPMC4754796
OpenAlexW2412853043

What OpenQuestion holds

Textmetadata
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.