Evidence map›Paper›PMID 33465281›Full record

ArticleJournal of cellular and molecular medicine2021

miR-34a in extracellular vesicles from bone marrow mesenchymal stem cells reduces rheumatoid arthritis inflammation via the cyclin I/ATM/ATR/p53 axis.

Huaiguo Wu, Xike Zhou, Xuedong Wang, Wei Cheng, Xinjia Hu, Yueping Wang, Bing Luo, Wenjun Huang, Juan Gu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
5.1field-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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

Huaiguo WuCenter for Precision Medicine, Anhui No. 2 Provincial People's Hospital, Hefei, China.
Xike ZhouDepartment of Medical Laboratory Science, The Fifth People's Hospital of Wuxi, Nanjing Medical University, Wuxi, China.
Xuedong WangCenter for Precision Medicine, Anhui No. 2 Provincial People's Hospital, Hefei, China.ORCID 0000-0002-6996-8373
Wei ChengCenter for Precision Medicine, Anhui No. 2 Provincial People's Hospital, Hefei, China.
Xinjia HuCenter for Precision Medicine, Anhui No. 2 Provincial People's Hospital, Hefei, China.
Yueping WangCenter for Precision Medicine, Anhui No. 2 Provincial People's Hospital, Hefei, China.
Bing LuoCenter for Precision Medicine, Anhui No. 2 Provincial People's Hospital, Hefei, China.
Wenjun HuangCenter for Precision Medicine, Anhui No. 2 Provincial People's Hospital, Hefei, China.
Juan GuDepartment of Medical Laboratory Science, The Fifth People's Hospital of Wuxi, Nanjing Medical University, Wuxi, China.
Anhui Provincial Hospital · CNJiangnan University · CNJinan University · CNUniversity of Massachusetts Boston · US

Funding

Key Project in Natural Science Research in Higher Education Institutions of Anhui Province KJ2018A0814Key Project in Natural Science Research in Higher Education Institutions of Anhui Province KJ2019A1096Natural Science Foundation of Jiangsu Province BK20181133Scientific Research Project of Anhui Provincial Health and Family Planning Commision 2018SEYL008
6 · The paper itself

Abstract

Extracellular vesicles (Evs) participate in the development of rheumatoid arthritis (RA), but the mechanisms remain unclear. This study aimed to determine the mechanism by which microRNA-34a (miR-34a) contained in bone marrow mesenchymal stem cell (BM-MSC)-derived Evs functions in RA fibroblast-like synoviocytes (RA-FLSs). BM-MSC-derived Evs and an Evs inhibitor were extracted. A rat model of RA was established. miR-34a gain- and loss-of-function experiments were performed, and the inflammation in rat synovial fluid and tissues was detected. The role of miR-34a in RA-FLSs was also measured in vitro. The target gene of miR-34a was predicted using the online software TargetScan and identified using a dual-luciferase reporter gene assay, and the activation of the ATM/ATR/p53 signalling pathway was assessed. BM-MSC-derived Evs mainly elevated miR-34a expression, which reduced RA inflammation in vivo and inhibited RA-FLS proliferation and resistance to apoptosis in vitro, while inhibited miR-34a expression enhanced RA development. In addition, miR-34a could target cyclin I to activate the ATM/ATR/p53 signalling pathway, thus inhibiting abnormal RA-FLS growth and RA inflammation. Our study showed that miR-34a contained in BM-MSC-derived Evs could reduce RA inflammation by inhibiting the cyclin I/ATM/ATR/p53 signalling pathway.

Indexed as

Gene Expression RegulationSignal TransductionAnimalsApoptosisArthritis, RheumatoidBiomarkersBiopsyCells, CulturedCyclin IExtracellular VesiclesMaleMesenchymal Stem CellsMicroRNAsRatsSynoviocytesTumor Suppressor Protein p53BiomarkersCyclin IMicroRNAsTumor Suppressor Protein p53ATM/ATR/p53 signalling pathwayCyclin Iextracellular vesiclesinflammationMicroRNA-34arheumatoid arthritis

Identifiers

PMID33465281
PMCPMC7882978
OpenAlexW3121558959

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.