Evidence map›Paper›PMID 31378783›Full record

ArticleCell death & disease2019

Asymmetrical methyltransferase PRMT3 regulates human mesenchymal stem cell osteogenesis via miR-3648.

Zhang Min, Liu Xiaomeng, Li Zheng, Du Yangge, Liu Xuejiao, Lv Longwei, Zhang Xiao, Liu Yunsong, Zhang Ping, Zhou Yongsheng

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. [Advances in oral and craniofacial bone regeneration modulated by stem cells and biomaterials].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026
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  10. PRMT7-Mediated PTEN Activation Enhances Bone Regeneration in Female Mice.International journal of molecular sciences · 2025
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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

10 authors at 2 institutions in 2 countries.

Zhang MinDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, 100081, Beijing, China.
Liu XiaomengBeijing Advanced Innovation center for Genomics (ICG), College of Life Sciences, Peking University, 100871, Beijing, China.
Li ZhengDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, 100081, Beijing, China.
Du YanggeDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, 100081, Beijing, China.
Liu XuejiaoDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, 100081, Beijing, China.
Lv LongweiDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, 100081, Beijing, China.
Zhang XiaoDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, 100081, Beijing, China.
Liu YunsongDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, 100081, Beijing, China.
Zhang PingDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, 100081, Beijing, China. zhangping332@bjmu.edu.cn.
Zhou YongshengDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, 100081, Beijing, China. kqzhouysh@hsc.pku.edu.cn.ORCID http://orcid.org/0000-0002-4332-0878
Peking University · CNKing University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone arginine methylation, which is catalyzed by protein arginine methyltransferases (PRMTs), plays a key regulatory role in various biological processes. Several PRMTs are involved in skeletal development; however, their role in the osteogenic differentiation of mesenchymal stem cells (MSCs) is not completely clear. In this study, we aimed to elucidate the function of PRMT3, a type-I PRMT that catalyzes the formation of ω-mono- or asymmetric dimethyl arginine, in MSCs osteogenesis. We found that PRMT3 promoted MSCs osteogenic commitment and bone remodeling. PRMT3 activated the expression of miR-3648 by enhancing histone H4 arginine 3 asymmetric dimethylation (H4R3me2a) levels at promoter region of the gene. Overexpression of miR-3648 rescued impaired osteogenesis in PRMT3-deficient cells. Moreover, administration of Prmt3 shRNA or a chemical inhibitor of PRMT3 (SGC707) caused an osteopenia phenotype in mice. These results indicate that PRMT3 is a potential therapeutic target for the treatment of bone regeneration and osteopenia disorders.

Indexed as

AnimalsBone Diseases, MetabolicBone RegenerationCell DifferentiationFemaleGene Knockdown TechniquesHEK293 CellsHistonesHumansIsoquinolinesMesenchymal Stem CellsMethylationMiceMice, Inbred C57BLMice, NudeMicroRNAsHistonesIsoquinolinesMicroRNAsMIRN3648-1 microRNA, humanPRMT3 protein, humanPRMT3 protein, mouseProtein-Arginine N-MethyltransferasesSGC707

Identifiers

PMID31378783
PMCPMC6680051
OpenAlexW2965190450

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.