Evidence map›Paper›PMID 26935950›Full record

ArticleOpen biology2016

TNF-α-induced NF-κB activation upregulates microRNA-150-3p and inhibits osteogenesis of mesenchymal stem cells by targeting β-catenin.

Nan Wang, Zubin Zhou, Tianyi Wu, Wei Liu, Peipei Yin, Chenhao Pan, Xiaowei Yu

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Open biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 87 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Nan WangDepartment of Orthopaedic Surgery, Shanghai Jiao Tong University affiliated Sixth People's Hospital, Shanghai, People's Republic of China Department of Emergency, the first affiliated hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Zubin ZhouDepartment of Orthopaedic Surgery, Shanghai Jiao Tong University affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Tianyi WuDepartment of Orthopaedics and Traumatology, Lui Che Woo Institute of Innovative Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong SAR, People's Republic of China.
Wei LiuDepartment of Orthopaedic Surgery, Shanghai Jiao Tong University affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Peipei YinDepartment of Orthopaedic Surgery, Shanghai Jiao Tong University affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Chenhao PanDepartment of Orthopaedic Surgery, Shanghai Jiao Tong University affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Xiaowei YuDepartment of Orthopaedic Surgery, Shanghai Jiao Tong University affiliated Sixth People's Hospital, Shanghai, People's Republic of China yuxw@sjtu.edu.cn.
Shanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CNChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although systemic or local inflammation, commonly featured by cytokine activation, is implicated in patients with bone loss, the underlying mechanisms are still elusive. As microRNAs (miR), a class of small non-coding RNAs involved in essential physiological processes, have been found in bone cells, we aimed to investigate the role of miR for modulating osteogenesis in inflammatory milieu using human bone marrow mesenchymal stem cells (hBM-MSCs). Induced by proinflammatory cytokine TNF-α, miR-150-3p was identified as a key player in suppressing osteogenic differentiation through downregulating β-catenin, a transcriptional co-activator promoting bone formation. TNF-α treatment increased the levels of miR-150-3p, which directly targeted the 3'-UTR of β-catenin mRNA and in turn repressed its expression. In addition, we observed that miR-150-3p expression was increased by TNF-α via IKK-dependent NF-κB signalling. There are three putative NF-κB binding sites in the promoter region of miR-150, and we identified -686 region as the major NF-κB binding site for stimulation of miR-150 expression by TNF-α. Finally, the osteogenic differentiation of hBM-MSCs was inhibited by either miR-150-3p overexpression or TNF-α treatment, which was prevented by anti-miR-150-3p oligonucleotides. Taken together, our data suggested that miR-150-3p integrated inflammation signalling and osteogenic differentiation and may contribute to the inhibition effects of inflammation on bone formation, thus expanding the pathophysiological functions of microRNAs in bone diseases.

Indexed as

Osteogenesisbeta CateninCell DifferentiationCells, CulturedGene Expression RegulationHumansMesenchymal Stem CellsMicroRNAsNF-kappa BOsteoblastsRNA, MessengerTumor Necrosis Factor-alphaUp-Regulationbeta CateninMicroRNAsMIR150, humanNF-kappa BRNA, MessengerTumor Necrosis Factor-alphamesenchymal stem cellsmicroRNAosteogenesisTNF-αβ-catenin

Identifiers

PMID26935950
PMCPMC4821240
OpenAlexW2289092264

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.