Evidence map›Paper›PMID 33995992›Full record

ArticleTherapeutic advances in chronic disease2021

MicroRNA-21 from bone marrow mesenchymal stem cell-derived extracellular vesicles targets TET1 to suppress KLF4 and alleviate rheumatoid arthritis.

Guo-Qing Li, Yu-Xuan Fang, Ying Liu, Fan-Ru Meng, Xia Wu, Chun-Wang Zhang, Yu Zhang, Yan-Qing Liu, Dan Liu

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

Article in Therapeutic advances in chronic disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.0field-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

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

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  13. Mesenchymal Stem Cells-Involved Strategies for Rheumatoid Arthritis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
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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 2 institutions in 1 country.

Guo-Qing LiDepartment of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, P. R. China.
Yu-Xuan FangDepartment of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, P. R. China.
Ying LiuClinical Medical College, Dalian Medical University, Dalian, P. R. China.
Fan-Ru MengClinical Medical College, Dalian Medical University, Dalian, P. R. China.
Xia WuClinical Medical College, Dalian Medical University, Dalian, P. R. China.
Chun-Wang ZhangClinical Medical College, Dalian Medical University, Dalian, P. R. China.
Yu ZhangMedical College of Yangzhou University, Yangzhou, P. R. China.
Yan-Qing LiuMedical College of Yangzhou University, Yangzhou, P. R. China.
Dan LiuDepartment of Pathology, Clinical Medical College, Yangzhou University, No. 98, Nantong West Road, Yangzhou, Jiangsu Province 225001, P. R. China.ORCID https://orcid.org/0000-0002-2724-1491
Dalian Medical University · CNYangzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccumulating evidence has demonstrated that bone marrow mesenchymal stem cells (BMSCs)-derived extracellular vesicles (EVs) can be used effectively to transfer drugs and biomolecules to target lesions. Meanwhile, BMSCs have been reported to be beneficial in the treatment of rheumatoid arthritis (RA). In this study, we employ gain- and loss-of-function experiments to determine how BMSCs-derived EVs alleviate RA

methodsWe isolated EVs from BMSCs and characterized them by transmission electron microscopy and western blot analysis. The regulatory relationship between miR-21 and TET1 was predicted by bioinformatics analysis and validated by dual luciferase assay. Next, we utilized bisulfite sequencing PCR to decipher how TET1 promoted KLF4 transcription. Then, we established an RA mouse model and determined the role of miR-21 in RA progression. Functional assays were used to validate the role the miR-21-TET1-KLF4 regulatory axis in controlling mouse fibroblast-like synoviocytes (mFLS) cell proliferation and inflammatory cytokines secretion

resultsRT-qPCR results revealed that miR-21 was highly expressed in BMSCs-derived EVs, and confirmed that BMSCs-derived EVs transferred miR-21 into mFLS cells. Bioinformatic analysis predicted that TET1 was the directly downstream target of miR-21, which was further validated by dual luciferase assay. TET1 promoted KLF4 promoter methylation to increase its expression. Collectively, BMSCs-derived EVs relieved RA by delivering miR-21, while the exosomal miR-21 alleviated RA through targeting the TET1/KLF4 regulatory axis.

conclusionmiR-21 from BMSCs-derived EVs suppresses KLF4 to relive RA by targeting TET1.

Indexed as

bone mesenchymal stem cellsextracellular vesiclesKrupple-like factor 4methylationmouse fibroblast-like synoviocytesrheumatoid arthritisten eleven translocation 1

Identifiers

PMID33995992
PMCPMC8072656
OpenAlexW3158558006

What OpenQuestion holds

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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.