Evidence map›Paper›PMID 27399683›Full record

ArticleInternational journal of molecular sciences2016

MicroRNA-146a-5p Negatively Regulates Pro-Inflammatory Cytokine Secretion and Cell Activation in Lipopolysaccharide Stimulated Human Hepatic Stellate Cells through Inhibition of Toll-Like Receptor 4 Signaling Pathways.

Yuhan Chen, Zhaochong Zeng, Xiaoyun Shen, Zhifeng Wu, Yinying Dong, Jason Chia-Hsien Cheng

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
3.5field-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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
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  14. MiRNA-146a-A Key Player in Immunity and Diseases.International journal of molecular sciences · 2023
    Review
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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

6 authors at 4 institutions in 2 countries.

Yuhan ChenDepartment of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai 200032, China. cspnr1@126.com.
Zhaochong ZengDepartment of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai 200032, China. zeng.zhaochong@zs-hospital.sh.cn.
Xiaoyun ShenDepartment of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai 200032, China. shen.xiaoyun@zs-hospital.sh.cn.
Zhifeng WuDepartment of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai 200032, China. wuzhifeng2@126.com.
Yinying DongDepartment of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai 200032, China. dongyinyingfd_1@163.com.
Jason Chia-Hsien ChengDivision of Radiation Oncology, Departments of Oncology, National Taiwan University Hospital, Taipei 100, Taiwan. jasoncheng@ntu.edu.tw.
Sun Yat-sen University · CNZhongshan Hospital · CNFudan University · CNNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipopolysaccharide (LPS)/toll-like receptor 4 (TLR4) signaling pathway is demonstrated to be involved in the hepatic fibrosis. MicroRNA (miR)-146a-5p is a key regulator of the innate immune response. The functional significance of miR-146a-5p during the LPS/TLR4 mediated hepatic fibrosis process remains unclear. In this study, we found that TLR4 and α-smooth muscle actin (α-SMA) were up-regulated and miR-146a-5p was down-regulated in human hepatic stellate cell (HSC) line LX2 after LPS stimulation. Overexpression of miR-146a-5p inhibited LPS induced pro-inflammatory cytokines secretion through down-regulating the expression levels of TLR-4, IL-1 receptor-associated kinase 1 (IRAK1), TNF receptor associated factor-6 (TRAF6) and phosphorylation of nuclear factor-kappa B (NF-κB). Knockdown of IRAK1 and TRAF6 also suppressed pro-inflammatory cytokine production by inhibiting NF-κB phosphorylation. In addition, miR-146a-5p mimic blocked LPS induced TRAF6 dependent c-Jun N-terminal kinase (JNK) and Smad2 activation as well as α-SMA production. Taken together, these results suggest that miR-146a-5p suppresses pro-inflammatory cytokine secretion and cell activation of HSC through inhibition of TLR4/NF-κB and TLR4/TRAF6/JNK pathway.

Indexed as

ActinsAntagomirsCells, CulturedCytokinesDown-RegulationEnzyme-Linked Immunosorbent AssayHepatic Stellate CellsHumansInterleukin-1 Receptor-Associated KinasesJNK Mitogen-Activated Protein KinasesLipopolysaccharidesMicroRNAsNF-kappa BPhosphorylationRNA InterferenceRNA, Small InterferingACTA2 protein, humanActinsAntagomirsCytokinesInterleukin-1 Receptor-Associated KinasesJNK Mitogen-Activated Protein KinasesLipopolysaccharidesMicroRNAsNF-kappa BRNA, Small InterferingSmad2 ProteinTNF Receptor-Associated Factor 6Toll-Like Receptor 4hepatic fibrosisinflammationmicroRNA-146atoll like receptor 4

Identifiers

PMID27399683
PMCPMC4964452
OpenAlexW2463612608

What OpenQuestion holds

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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.